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

2. Course Abstract An overview of anterior segment disorders
Review of clinical signs
Consideration on differential diagnosis
Current treatment and management modalities

3. Red Eye Etiologies Infection Inflammation Irritation Allergy Trauma
Chemicals
Tumor
Systemic conditions

4. Systematic Evaluation of the Red Eye
Orbit
Lids
Lacrimal system
Conjunctiva and sclera
Cornea
Anterior chamber
Iris and pupil
Retina and optic nerve

5. Red Eye Disorders: Non-Vision Threatening
Blepharitis
Hordeolum
Chalazion
Conjunctivitis
Dry eyes
Corneal abrasions
Subconjunctival hemorrhage

6. Blepharitis Colonization of margin with staphylococcus
Classic sign is fibrin collarette
May lead to loss of lashes and margin ulcerations if severe and chronic

7. Blepharitis Staph blepharitis may occur with seborrhea.
Often may develop associated problems.
Marginal infiltrates.
Hordeolum.
Chalazion.
Meibomitis.

8. 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

9. 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

10. 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

11. CHALAZION EXCISION

12. MEIBOMITIS
Meibomian orifice shows erythema and edema with secretions thick and tenacious
Often diffusely inflamed lid margins
Oral teracycline helpful (doxy 100 BID)

13. 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

14. 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

15. 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

16. 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.

17. CONJUNCTIVITIS
Allergic
Viral
Bacterial
Chemical/toxic

18. 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.

19. 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

20. 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.

21. 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.

22. VIRAL CONJUNCTIVITIS
Adenoviral conjunctivitis presents with acute onset of red, watery eyes.
Follicular response worse inferiorly.
Hemorrhagic or pseudomembranous response can occur.

23. Adenoviral Conjunctivitis
Development of pseudomembranes and symblepharon can occur and delays healing.
Highly contagious and usually lasting 10 days.
Large ,rapidly spreading epidemics.

24. Adenoviral Associated Keratitis

25. Adenoviral Keratitis
Represent sterile immunological reactions to viral antigen. Except early
Can produce a severe prolonged subepithelial keratitis which profoundly drops Va

26. 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.

27. BACTERIAL CONJUNCTIVITIS
HYPERACUTE: Neisseia gonorrhea
Acute catarrhal: s. Pneumonia, Staph, H. . Aegypticus
SUBACUTE: h.Flu
CHRONIC: Staph, Moraxella, pseudomonas,gram negs

28. 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.

29. Traumatic Subconjunctival Hemorrhage

30. 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.

31. 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

32. 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 hours.
Recurrent erosions may be sequela of traumatic abrasions.

33. Corneal Abrasion

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

35. Pseudomonas Ulcer Post Patching Corneal Abrasion

36. 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

37. 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

38. 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.

39. 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

40. Pterygium

41. 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

42. 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.

43. Pterygium and Pinguecula Treatment
Lubrication - tears
Topical vasoconstrictors
Topical NSAIDs
Topical steroids (not recommended for long term use)
Surgical excision

44. 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

45. Red Eye Disorders: Vision Threatening
Orbital Cellulitis
Scleritis
Uveitis
Trauma
Hyphema
Acute glaucoma
Corneal infections

46. 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.

47. Orbit: Preseptal Cellulitis
Erythema of lids
Edema of lids
Tenderness
Fever
Normal vision
Motility normal
No proptosis

48. Preseptal Cellulitis

49. 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.

50. Orbital Cellulitis Infection extends posterior to the septum
Medical emergency !
Vision threatening
Life-threatening
Consult with ENT, ophthalmology, infectious disease necessary

51. ORBITAL CELLULITIS

52. Orbital Cellulitis Lid swelling and erythema +/- Proptosis
+/- Conjunctival chemosis and/or injection
Reduced motility
Pain
Fever
+/- Optic nerve: decreased vision, APD, disc edema

53. Orbital Cellulitis

54. Orbital Cellulitis

55. Orbital Cellulitis Management
Hospitalization
CT scan of head, orbits, and sinuses
Blood cultures
Possible spinal fluid evaluation - LP
Consult ENT, ophthalmology, and infectious disease

56. Orbital Cellulitis Treatment & Complications
IV antibiotics: staphylococcus, streptococcus, H. influenzae
Surgical debridement if fungus, no improvement,or subperiosteal abscess
Complications: meningitis, cavernous sinus thrombosis

57. Episcleritis and Scleritis
Inflammatory conditions
Redness and tenderness
Localized or diffuse
Etiologies: idiopathic, inflammatory (autoimmune) , infectious

58. 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

59. Episcleritis Treatment
Topical vasoconstrictor
Topical NSAID
Topical steroid
Systemic NSAID
If recurrent, consider systemic work up for infectious or autoimmune etiologies

60. 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.

61. Scleritis Classification
Anterior
Posterior
Both
Diffuse
Nodular
Necrotizing
Non –necrotizing ie. Scleromalacia Perforans

62. Symptoms of Scleritis
Periocular pain
Headache
Visual loss
Red eye

63. Scleritis Severe potentially destructive disorder. Usually age 20-60.
Women> men.
Moderately to severely painful.
Violaceous hue ,gradual onset with Scleral edema.

64. Scleritis Deep episcleral plexus is immobile, bluish red.
Deep pain is common .
Tender to palpation.
Nodular anterior scleritis: may have multiple nodules in 40%.

65. Scleromalacia Perforans
Usually associated with long standing rheumatoid arthritis.
Progressive scleral thinning without signs of inflammation.
Large abnormal vessels cross the devitalized area.

66. Scleromalacia Perforans
Bulging Staphylomas can develop.

67. 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

68. 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

69. 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%)

70. Posterior Scleritis McCluskey - Ophthalmology 1999 (137 patients)
Glaucoma (12%)
Uveitis (4%)
Retinal Vasculitis (2%)
RPE changes (2%)

71. Posterior Scleritis Presents with: Pain. Proptosis. Decreased Va.
Occasionally motility disturbances.
CHOROIDAL FOLDS can occur.

72. Posterior Scleritis
Imaging studies may demonstrate thickened posterior sclera.
Often useful in making the diagnosis.

73. Scleritis Treatment Diffuse or nodular Scleritis: Oral NSAID initially
indomethacin 75mg BID
naproxen mg BID
Ibuprofen mg QID
piroxicam 20mg daily
sulindac 200mg BID
In case of therapeutic failure: steroids prednisone mg daily with rapid taper

74. 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

75. Complications of Scleritis
Keratitis
Cataract
Uveitis
Glaucoma
Scleral thinning

76. 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.

77. Corneal Disorders with Associated Red Eye
Symptoms include:
Pain
Foreign body sensation
Photophobia
Blurred vision

78. 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

79. Metallic Corneal Foreign Body
Look for signs of perforation if acceleration injury eg. Grinding or drilling.
Use topical broad spectrum antibiotics after removal.

80. Chemical Injury True ocular emergency
Requires immediate irrigation with nearest source of water
Management dependent on acid or alkaline offending substance

81. Chemical Injury: Acid Extent of damage produced immediately
Precipitates protein
Usually self limited except fot the strongest of acids

82. 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

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

84. Alkaline Injury
Epithelial disintegration followed by stromal ulceration.
Limbal region burns have worse prognosissince pluripotential limbal stem cells are lost.

85. Sequela of Alkali Burns

86. Chemical Burns: Management
Immediate irrigation
Topical antibiotics
Cycloplegia
Removal of particulate matter eg. Fertilizer
Goal is to reepithelialize the cornea

87. 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.

88. 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.

89. 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

90. 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.

91. 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.

92. 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.

93. 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

94. 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.

95. Uveitis Limbal (circumcorneal) flush (redness) Pain Photophobia
Decreased vision
Pupillary abnormalities
AC Rxn possibly hypopyon

96. Uveitis

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

98. Uveitis
Treatment includes: cycloplegia, topical steroids, possible systemic immunosuppressive medications
Treatment is aimed at reducing inflammation to prevent glaucoma, cataracts, and macula edema

99. 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

100. 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

101. Pupillary Block Mechanism

102. Peripheral Iridectomy

103. Red Eye Management Timely, accurate diagnosis
Appropriate referral when indicated
Knowledge of each entity makes correct diagnosis and treatment likely