Management of the Red Eye Anthony Cavallerano, OD VA Boston Health Care System New England College...
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Transcript of Management of the Red Eye Anthony Cavallerano, OD VA Boston Health Care System New England College...
Management of the Red Eye
Anthony Cavallerano, OD
VA Boston Health Care System
New England College of Optometry
Boston, Massachusetts
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