Transcript Management of the Red Eye

Management of the
Red Eye
Anthony Cavallerano, OD
VA Boston Health Care System
New England College of Optometry
Boston, Massachusetts
[email protected]
Course Abstract
An overview of anterior segment
disorders
 Review of clinical signs
 Consideration on differential diagnosis
 Current treatment and management
modalities
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Red Eye Etiologies
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Infection
Inflammation
Irritation
Allergy
Trauma
Chemicals
Tumor
Systemic conditions
Systematic Evaluation of the
Red Eye
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Orbit
Lids
Lacrimal system
Conjunctiva and sclera
Cornea
Anterior chamber
Iris and pupil
Retina and optic nerve
Red Eye Disorders: NonVision Threatening
Blepharitis
 Hordeolum
 Chalazion
 Conjunctivitis
 Dry eyes
 Corneal abrasions
 Subconjunctival hemorrhage
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Blepharitis
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Colonization of margin with
staphylococcus
Classic sign is fibrin
collarette
May lead to loss of lashes
and margin ulcerations if
severe and chronic
Blepharitis
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Staph blepharitis
may occur with
seborrhea.
Often may develop
associated
problems.
Marginal infiltrates.
Hordeolum.
Chalazion.
Meibomitis.
Marginal infiltrates.
Acute Hordeolum
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Acute staph infection of
lid
External-glands of
Zeiss, moll or lash
follicle
Internal- Meibomian
Warm compresses
Systemic antibiotics if
preseptal cellulitis
develops
Chalazion
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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
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CHALAZION EXCISION
MEIBOMITIS
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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
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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
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Phlyctenulosis
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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.
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CONJUNCTIVITIS
 Allergic
 Viral
 Bacterial
 Chemical/toxic
Allergic Conjunctivitis
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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
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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
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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 TOPICALLYusecautiously but often needed since
it can be extremely uncomfortable and
Va may be decreased.
 No steroids in between attacks.
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VIRAL CONJUNCTIVITIS
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Adenoviral conjunctivitis
presents with acute onset
of red, watery eyes.
Follicular response worse
inferiorly.
Hemorrhagic or
pseudomembranous
response can occur.
Adenoviral Conjunctivitis
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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
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Represent sterile
immunological
reactions to viral
antigen. Except
early
Can produce a
severe prolonged
subepithelial
keratitis which
profoundly drops
Va
ADENOVIRUS
TREATMENT
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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
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Bacterial Conjunctivitis
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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
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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
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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.
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Corneal Abrasion
Corneal Abrasion Therapy
Foster rapid healing
 Restore patient comfort
 Prevent secondary infections
 Topical cycloplegic to relieve pain
 Topical antibiotic
 +/- Patch, +/- bandage lens
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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
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DRY EYE SYNDROME
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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 :
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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,an
d arthritis usually in
middle aged women.
Tear replacement,
plugs, rarely lateral
tarsorraphy.
Pinguecula
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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
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Pterygium
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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
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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
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Red Eye Disorders: Vision
Threatening
Orbital Cellulitis
 Scleritis
 Uveitis
 Trauma
 Hyphema
 Acute glaucoma
 Corneal infections
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Preseptal Cellulitis
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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
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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.
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Orbital Cellulitis
Infection extends posterior to the
septum
 Medical emergency !
 Vision threatening
 Life-threatening
 Consult with ENT, ophthalmology,
infectious disease necessary
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ORBITAL
CELLULITIS
Orbital Cellulitis
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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
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Orbital Cellulitis Treatment
& Complications
IV antibiotics: staphylococcus,
streptococcus, H. influenzae
 Surgical debridement if fungus, no
improvement,or subperiosteal
abscess
 Complications: meningitis,
cavernous sinus thrombosis
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Episcleritis and Scleritis
Inflammatory conditions
 Redness and tenderness
 Localized or diffuse
 Etiologies: idiopathic, inflammatory
(autoimmune) , infectious
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Episcleritis
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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
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Episcleritis
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Straight radial inflamed vessels.
Salmon pink and movable
vessels.
Blanch with adrenergic agents
as opposed to scleral vessels.
Minimal to no pain.
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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
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Anterior
Posterior
Both
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Diffuse
Nodular
Necrotizing
Non –necrotizing
ie. Scleromalacia
Perforans
Symptoms of Scleritis
Periocular pain
 Headache
 Visual loss
 Red eye
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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
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Systemic diseases
associated with scleritis
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Rheumatoid Arthritis
Systemic vasculitis
Wegener Granulomatosis
Vogt Koyangi-Harada
disease
Thyroid disease
Sarcoidosis
Systemic Lupus
erythematosus
Inflammatory Bowel
Disease
Multiple Myeloma
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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%)
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Posterior Scleritis
McCluskey - Ophthalmology 1999
(137 patients)
Glaucoma (12%)
 Uveitis (4%)
 Retinal Vasculitis (2%)
 RPE changes (2%)
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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
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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
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In case of therapeutic failure:
immunosuppressive drugs:
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cyclophosphamide 1 -2 mg/kg daily
azathioprine 1 -2 mg/kg daily
cyclosporine 3 -5 mg/kg daily
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Complications of Scleritis
Keratitis
 Cataract
 Uveitis
 Glaucoma
 Scleral thinning
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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.
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Corneal Disorders with
Associated Red Eye
Symptoms include:
 Pain
 Foreign body sensation
 Photophobia
 Blurred vision
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Corneal & Conjunctival
Foreign Body
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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
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Chemical Injury: Acid
Extent of damage produced
immediately
 Precipitates protein
 Usually self limited except fot the
strongest of acids
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Acute Alkaline Injury :
Ammonia
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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
mucopolysaccharid
e 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
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Alkali Burn Management
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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.
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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
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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.
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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
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
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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
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Limbal (circumcorneal)
flush (redness)
Pain
Photophobia
Decreased vision
Pupillary abnormalities
AC Rxn possibly
hypopyon
Uveitis
Uveitis Evaluation
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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
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Acute Angle Closure
Glaucoma
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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
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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
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