Management of the Red Eye

Anthony Cavallerano, OD

VA Boston Health Care System

New England College of Optometry

Boston, Massachusetts

Anthony.cavallerano@va.gov

Course Abstract

An overview of anterior segment disorders

Review of clinical signs Consideration on differential diagnosis Current treatment and management

modalities

Red Eye Etiologies

Infection Inflammation Irritation Allergy Trauma Chemicals Tumor Systemic conditions

Systematic Evaluation of the Red Eye

Orbit Lids Lacrimal system Conjunctiva and sclera Cornea Anterior chamber Iris and pupil Retina and optic nerve

Red Eye Disorders: Non-Vision Threatening

Blepharitis Hordeolum Chalazion Conjunctivitis Dry eyes Corneal abrasions Subconjunctival hemorrhage

Blepharitis

Colonization of margin with staphylococcus

Classic sign is fibrin collarette

May lead to loss of lashes and margin ulcerations if severe and chronic

Blepharitis

Staph blepharitis may occur with seborrhea.

Often may develop associated problems.

Marginal infiltrates. Hordeolum. Chalazion. Meibomitis. Marginal infiltrates.

Acute Hordeolum

Acute staph infection of lid

External-glands of Zeiss, moll or lash follicle

Internal- Meibomian Warm compresses Systemic antibiotics if

preseptal cellulitis develops

Chalazion

Obstruction of Meibomian gland with extrusion of lipid into surrounding tissue

Lipogranulomatous reaction, not infectious

May cause astigmatism secondary to pressure on the cornea

CHALAZION TREATMENT

Most slowly shrink and disappear Warm compresses Massage with compression to express

contents thru the Meibomian orifice Oral tetracycline may hasten

resolution secondary to its lipid transforming capability

EXCISION usually from conj side

CHALAZION EXCISION

MEIBOMITIS

Meibomian orifice shows erythema and edema with secretions thick and tenacious

Often diffusely inflamed lid margins

Oral teracycline helpful (doxy 100 BID)

STAPH MARGINAL INFILTRATES

Usually non staining discrete limbal infiltrates which are immune mediated and non infectious

Must first rule out infectious keratitis before using steroids

Treat underlying cause ie. blepharitis

Blepharitis treatment

Lid hygiene, as often as possible Antibiotic ointment to lid margins after

cleaning ie. Bacitracin, erythromycin,rarely sulfacetamide

Lubrication often relieves the foreign body sensation which often accompanies the entity

Phlyctenulosis

Round elevated infiltrate which moves centrally from limbus with “leash of vessels”

Sterile type IV hypersensitivity immune rxn , usually to Staph but may be secondary to T.B., or fungal infections

Phlyctenule Usually resolves spontaneously in 10 –14

days. Photophobia ,tearing and pain. Usually leaves pannus and scarring but

can rarely perforate. Topical steroids are used but treating the

underling cause is essential.

CONJUNCTIVITIS

AllergicViral BacterialChemical/toxic

Allergic Conjunctivitis

Usually allergy to air born allergen.

Mediated by IgE. May occur with hay fever,

asthma or rhinitis. Associated with itching,

hyperemia, chemosis, watery ,mucoid discharge.

Topical vasoconstrictors and mast cell stabilizers helpful.

VERNAL CONJUNCTIVITIS

Seasonally recurring History of atopy common Occurs in children and

young adults Hyperemia and chemosis

progress to diffuse papillary hypertrophy on upper tarsus

VERNAL SHIELD ULCER

Localized oval or pentagonal lesion in upper cornea can develop.

Limbal vernal with papilla and Horner-Trantas dots can occur , usually in blacks.

VERNAL CONJUNCTIVITIS

Cold compresses. Topical vasoconstrictors. STEROIDS TOPICALLY-

usecautiously but often needed since it can be extremely uncomfortable and Va may be decreased.

No steroids in between attacks.

VIRAL CONJUNCTIVITIS

Adenoviral conjunctivitis presents with acute onset of red, watery eyes.

Follicular response worse inferiorly.

Hemorrhagic or pseudomembranous response can occur.

Adenoviral Conjunctivitis

Development of pseudomembranes and symblepharon can occur and delays healing.

Highly contagious and usually lasting 10 days.

Large ,rapidly spreading epidemics.

Adenoviral Associated Keratitis

Adenoviral Keratitis

Represent sterile immunological reactions to viral antigen. Except early

Can produce a severe prolonged subepithelial keratitis which profoundly drops Va

ADENOVIRUS TREATMENT INFORM patient of 2-4 week course. May get worse before better. HIGHLY CONTAGIOUS – precautions. Tears or topical vasoconstrictors. Antibiotics if secondarily infected. Remove pseudomembranes. Cifovidir? Not FDA approved as of yet. Topical steroids for SEI’S.

BACTERIAL CONJUNCTIVITIS

HYPERACUTE: Neisseia gonorrhea Acute catarrhal: s. Pneumonia,

Staph, H. . Aegypticus SUBACUTE: h.Flu CHRONIC: Staph, Moraxella,

pseudomonas,gram negs

Bacterial Conjunctivitis

Mucopurulent discharge.

Broad spectrum antibiotics hasten the resolution.

Must consider gonococcus since it can cause a perforation-hyperacute, needs systemic antibiotics. And has a preauricular node like Adeno.

Traumatic Subconjunctival Hemorrhage

Subconjunctival Hemorrhage Bright blood red eye. Normal vision. No pain. Usually no obvious cause, often told by

others that “eye is red.” May occur in cases of trauma, or in cases of

coughing, vomiting, or straining. If traumatic must do thorough exam to R/O

other pathology.

Subconjunctival Hemorrhage Management

No therapy Reassurance that the condition is not

serious and will resolve in 1-3 weeks Hematologic coagulation studies are

not indicated unless there are associated retinal hemorrhages or many recurrences

Corneal Abrasions

Causes: injury, UV light (welder’s arc), contact lens related, corneal dystrophies, recurrent erosion syndrome, dry eye, corneal anesthesia, infections.

Trauma related abrasions heal very quickly, usually in 24-48 hours.

Recurrent erosions may be sequela of traumatic abrasions.

Corneal Abrasion

Corneal Abrasion Therapy

Foster rapid healing Restore patient comfort Prevent secondary infections Topical cycloplegic to relieve pain Topical antibiotic +/- Patch, +/- bandage lens

Pseudomonas Ulcer Post Patching Corneal Abrasion

Cornea Abrasion Management

Never patch a contact lens patient due to high risk of infection

Never prescribe topical anesthetics for pain control because of the toxic effects on the corneal epithelium

DRY EYE SYNDROME

Symptoms of tear deficiency include; FB sensation Tearing Ropy mucus Burning Scratchiness ALL WORSE LATER IN THE DAY or in

HEAT< WIND OR LOW HUMIDITY

DRY EYE :

Schirmer testing can confirm-5 with,15 without anesthesia in 5 mins.

Rose Bengal staining. Tear BUT: ,10 secs is

definitely abnormal. Sjogrens syndome is

K.Sicca,xerostomia,and arthritis usually in middle aged women.

Tear replacement, plugs, rarely lateral tarsorraphy.

Pinguecula

Benign pathologic change in the bulbar conjunctiva at the palpebral fissure

Associated with sun and wind exposure

Red secondary to increased vascularity of the lesion

Can be intermittently inflamed

Pterygium

Pterygium

Benign change in the bulbar conjunctiva that extends onto the cornea, usually , although not restricted to the medial side of the cornea

Associated with wind and sun exposure Red secondary to the increased

vascularity of the lesion; easily irritated

Pterygium

Wing shaped fold of conj that invades superficial cornea, preceeded by pinguecula.

Increase with proximity to equator.

Elastoid degeneration of collagen with destruction of Bowmans.

Stocker’s line at the head of pterygium.

Pterygium and Pinguecula Treatment

Lubrication - tears Topical vasoconstrictors Topical NSAIDs Topical steroids (not recommended

for long term use) Surgical excision

Surgical Excision : Indications Encroachment on the visual axis Induced astigmatism Chronic irritation Recurrence rate varies from as high

as 50% to as low as 15% Bare sclera technique without

radiation or antifibrotics Free conjunctival grafts are helpful

Red Eye Disorders: Vision Threatening

Orbital Cellulitis Scleritis Uveitis Trauma Hyphema Acute glaucoma Corneal infections

Preseptal Cellulitis

Inflammation and infection cinfined to periorbital structures anterior to the septum.

In children, underlying sinusitis common eg. H. Flu.

In adults, oftensuperficial skin source is etiology eg. Staph Aureus.

Orbit: Preseptal Cellulitis

Erythema of lids Edema of lids Tenderness Fever Normal vision Motility normal No proptosis

Preseptal Cellulitis

Preseptal Cellulitis Treatment

Systemic antibiotics. Possible admission for pediatric

population with special attention to gram+ coverage and H. Flu.

Adults can be treated with oral antibiotics but watched closely for progression to orbital involvement.

Orbital Cellulitis

Infection extends posterior to the septum

Medical emergency ! Vision threatening Life-threatening Consult with ENT, ophthalmology,

infectious disease necessary

ORBITAL CELLULITIS

Orbital Cellulitis

Lid swelling and erythema +/- Proptosis +/- Conjunctival chemosis and/or injection Reduced motility Pain Fever +/- Optic nerve: decreased vision, APD,

disc edema

Orbital Cellulitis

Orbital Cellulitis

Orbital Cellulitis Management

Hospitalization CT scan of head, orbits, and sinuses Blood cultures Possible spinal fluid evaluation - LP Consult ENT, ophthalmology, and

infectious disease

Orbital Cellulitis Treatment & Complications

IV antibiotics: staphylococcus, streptococcus, H. influenzae

Surgical debridement if fungus, no improvement,or subperiosteal abscess

Complications: meningitis, cavernous sinus thrombosis

Episcleritis and Scleritis

Inflammatory conditions Redness and tenderness Localized or diffuse Etiologies: idiopathic, inflammatory

(autoimmune) , infectious

Episcleritis

May be benign or signify underlying disease

Red eye usually localized, but may be diffuse, or nodular

Dilated episcleral vessels Mild tenderness and

irritation

Episcleritis Treatment

Topical vasoconstrictor Topical NSAID Topical steroid Systemic NSAID If recurrent, consider systemic work

up for infectious or autoimmune etiologies

Episcleritis Straight radial inflamed vessels. Salmon pink and movable

vessels. Blanch with adrenergic agents

as opposed to scleral vessels. Minimal to no pain.

Sectorial 70%, Diffuse 30%. Does not progress to

scleritis. 2/3 have recurrences

but it usually clears without treatment.

Topical NSAID’s or rarely steroids to treat.

Scleritis Classification

Anterior Posterior Both

Diffuse Nodular Necrotizing Non –necrotizing

ie. Scleromalacia Perforans

Symptoms of Scleritis

Periocular pain Headache Visual loss Red eye

Scleritis

Severe potentially destructive disorder.

Usually age 20-60.Women> men.Moderately to

severely painful.Violaceous

hue ,gradual onset with Scleral edema.

Scleritis

Deep episcleral plexus is immobile, bluish red.

Deep pain is common .

Tender to palpation.Nodular anterior

scleritis: may have multiple nodules in 40%.

Scleromalacia Perforans

Usually associated with long standing rheumatoid arthritis.

Progressive scleral thinning without signs of inflammation.

Large abnormal vessels cross the devitalized area.

Scleromalacia Perforans

Bulging Staphylomas can develop.

Scleritis Evaluation

History Examination of anterior and posterior

segments B-scan Bloods: CBC with diff, SMA 18, ESR, RF,

ANA, c-anca, p-anca, VDRL/FTA PPD CXR

Systemic diseases associated with scleritis

Rheumatoid Arthritis Systemic vasculitis Wegener Granulomatosis Vogt Koyangi-Harada

disease Thyroid disease Sarcoidosis Systemic Lupus

erythematosus Inflammatory Bowel Disease Multiple Myeloma

Lymphoma Ankylosing Spondylitis Poly arteritis nodosa Primary Biliary cirrhosis Relapsing Polychondritis Reiters syndrome Psoriatic arthritis Ankylosing spondylitis Infectious diseases: TB;

syphillis; HSV; HZV; Other Idiopathaic

Posterior Scleritis McCluskey - Ophthalmology 1999 (137 patients)

Associated anterior scleritis (34%) Serous retinal detachment (21%) Swollen optic disc (18%) No abnormalities (17%) Subretinal localized granuloma (13%)

Posterior Scleritis McCluskey - Ophthalmology 1999 (137 patients)

Glaucoma (12%) Uveitis (4%) Retinal Vasculitis (2%) RPE changes (2%)

Posterior Scleritis

Presents with:

Pain.

Proptosis.

Decreased Va.

Occasionally motility disturbances.

CHOROIDAL FOLDS can occur.

Posterior Scleritis

Imaging studies may demonstrate thickened posterior sclera.

Often useful in making the diagnosis.

Scleritis Treatment

Diffuse or nodular Scleritis: Oral NSAID initially indomethacin 75mg BID naproxen 375-500mg BID Ibuprofen 400-600mg QID piroxicam 20mg daily sulindac 200mg BID In case of therapeutic failure:

steroids prednisone 60-120mg daily with rapid taper

Scleritis Treatment

In case of therapeutic failure: immunosuppressive drugs:

cyclophosphamide 1 -2 mg/kg daily azathioprine 1 -2 mg/kg daily cyclosporine 3 -5 mg/kg daily

Complications of Scleritis

Keratitis Cataract Uveitis Glaucoma Scleral thinning

Infectious Scleritis

Any case of a necrotizing scleritis needs to be evaluated for an infectious etiology including scrapings from the necrotic sites.

Gram stain; Blood, chocolate, Thioglycollate or meat infusion broth, and Sabaroud’s media.

Corneal Disorders with Associated Red Eye

Symptoms include: Pain Foreign body sensation Photophobia Blurred vision

Corneal & Conjunctival Foreign Body

Presents with c/o pain, tearing, photophobia and foreign body sensation

Foreign body (FB) may be flushed out if superficial, cotton tip after anesthetic

If not easily dislodged – can be removed with 25 gauge needle, rust ring with Alger brush

Subsequent defect to be treated with antibiotics

Flip lid if no FB seen and linear abrasion

Metallic Corneal Foreign Body

Look for signs of perforation if acceleration injury eg. Grinding or drilling.

Use topical broad spectrum antibiotics after removal.

Chemical Injury

True ocular emergency Requires immediate irrigation with

nearest source of water Management dependent on acid or

alkaline offending substance

Chemical Injury: Acid

Extent of damage produced immediately

Precipitates protein Usually self limited except fot the

strongest of acids

Acute Alkaline Injury : Ammonia

Causes damage long after initial contact

Saponifies tissues Can lead to corneal

opacification, melting, perforation, and severe glaucoma as a late complication

Acute Alkaline Injury

When ph is above 11.5, the mucopolysaccharide ground substance is is destroyed resulting in profound damage.

Alkaline Injury

Epithelial disintegration followed by stromal ulceration.

Limbal region burns have worse prognosissince pluripotential limbal stem cells are lost.

Sequela of Alkali Burns

Chemical Burns: Management

Immediate irrigation Topical antibiotics Cycloplegia Removal of particulate matter eg.

Fertilizer Goal is to reepithelialize the cornea

Alkali Burn Management

Coticosteroids topically can be used for the first 5-7 days as they combat the initial inflammatory process but may potentiate the collagenase activity.

Topical collagenase inhibitors eg. L-cysteine or acetylcysteine or EDTA may reduce collagenase induced stromal ulceration .

Surgical autologous conj . grafts folllowed by PK may be helpful.

Contact Lens Wear Associated Red Eye

Prolonged contact lens wear or poorly fitting lenses may cause a red eye.

Severe pain. Tearing. If opacity is noted or corneal infection

is suspected,treat as if infected. Bacterial, parasite, fungus are

possible pathogens.

Bacterial Keratitis

Red, painful eye Watery - purulent discharge May observe discrete corneal opacity May have decreased vision May have AC reaction &/or hypopyon Cultures of corneal ulceration Broad spectrum topical antibiotic

therapy

Bacterial Corneal Ulcer

Predisposing factors usually include trauma.

All may contribute:Immunosuppression.Alcoholism.Aging.Dry eye.Exposed sutures.Contact

lens wear.Bullous Keratopathy.Topical steroid use.

Treatment of Bacterial Keratitis Confirmation with scrapings and

cultures are essential. Gram stain. Initial broad spectrum treatment with

antibiotics eg. Flouroquinolone and Bacitracin, Cefazolin and Amikacin are indicated .

Modify treatment as culture results dictate.

Fungal Corneal Ulcer

Can mimic bacterial or viral keratitis.

Often occur after trauma with plant or vegetable matter.

Aspergillus, Fusarium and Penicillium occur in otherwise normal eyes wheras Candida occurs in immunocompromised anterior segments.

Natamycin5% is available.Bad prognosis ,may need

PK.

Viral Keratitis

HSV, HZV Usually unilateral Red, tearing, foreign body sensation Single or multiple branching lesions

(dendrites) highlight with fluorescein stain Systemic &/or topical antiviral therapy,

possible antibiotic therapy and cycloplegia

Viral Keratitis (HSV)

Replicates along the corneal nerves.

Decreased corneal sensation.

Heals spontaneously in 21 days but Trifluridine 8x/day hastens the process.

Avoid steroids unless DISCIFORM or KERATOUVEITIS occurs and then with 1:1antivirals.

Uveitis

Limbal (circumcorneal) flush (redness)

Pain Photophobia Decreased vision Pupillary abnormalities AC Rxn possibly

hypopyon

Uveitis

Uveitis Evaluation

Autoimmue and infectious work up CBC with differential ESR Ana Ace HLAB-27 VDRL/FTA CXR PPD

Uveitis

Treatment includes: cycloplegia, topical steroids, possible systemic immunosuppressive medications

Treatment is aimed at reducing inflammation to prevent glaucoma, cataracts, and macula edema

Acute Angle Closure Glaucoma Sudden rise in

intraocular pressure ( IOP)

Mid-dilated pupil Halos, decrease in

vision Pain Red eye Cloudy cornea (corneal

edema) Nausea and vomiting Headache

Acute Angle Closure Glaucoma Visually threatening High pressure can lead to optic nerve &/or

retinal damage, including, but not limited to vascular occlusions

Treatment is aimed at lowering IOP: topical beta-blocker, pilocarpine, apraclonidine, CAI, oral acetazolamide, oral glycerine or isosorbide

Definitive treatment: laser peripheral Iridectomy in both eyes

Pupillary Block Mechanism

Peripheral Iridectomy

Red Eye Management

Timely, accurate diagnosis Appropriate referral when indicated Knowledge of each entity makes

correct diagnosis and treatment likely