Disorders of the Eye

Educational Objectives

The goal of this program is to improve the awareness of current practice for the evaluation of red eye and dry eye by internists. After hearing and assimilating this program, the clinician will be better able to:

1. Identify common causes of red eye that may be seen in the clinic setting.
2. Distinguish between non-emergent and emergent causes of red eye and when to refer for ophthalmologic evaluation.
3. Distinguish between true dry eye and other eye conditions presenting with a dry eye sensation.

Summary

PDF of all summaries for this board review course

Approach to the Red Eye

Layers of eye surface:

Tear film: 3 layers; lipid outermost layer formed by Meibomian glands (within tarsal plate of eyelids), seals tears in; water component formed by lacrimal and accessory lacrimal glands (superotemporal); mucin layer formed by goblet cells to help tear film stick to eye; eyelids mix tear film into layers; blinking dissipates and reforms tear film; provides refractive surface and fights infection

Conjunctiva: flimsy tissue; covers white part of eye and lines innermost part of eyelids; bulbar conjunctiva covers white part of eye; palpebral conjunctiva lines eyelids; conjunctiva meets cornea at limbus; beneath conjunctiva are episclera and sclera; episclera has layer of blood vessels above white of eye; sclera has superficial blood vessels but avascular at deeper level

Red eye: consider layers from outside to inside

Ocular surface disease: disorders of tear film and superficial cornea; look for skin changes around eye (rosacea, seborrheic dermatitis), eyelid function; in ectropion, eyelid flapping out; in entropion, eyelid twisted in; look for laxity (common in sleep apnea); slit-lamp examination of lid margin for signs of blepharitis; anterior blepharitis has crust or collarette on lashes and eyes that causes red and scratchy eye; posterior blepharitis (Meibomian gland dysfunction) involves sebaceous glands in tarsal plate of conjunctiva and causes tears not to last long; anatomic disorders can cause tear film problems; conjunctivochalasis is degenerative change causing conjunctiva to become loose and drape over lower eyelid; check with slit-lamp and fluorescein strip; growths on eye can block flow of tears; pterygium is a common wing-like growth over cornea that is benign and related to sun exposure, can decrease vision if blocks pupil or cause astigmatism; should be examined to rule out malignancy

Subconjunctival hemorrhage: diffuse bleeding; dramatic but benign and resolves on its own; check blood pressure; usually does not progress; patients on blood thinners or who have had recent trauma or rubbing of eye are at risk

Bump on upper cornea: filtering surgery for glaucoma causes bleb or bump on top part of cornea; sometimes misdiagnosed as ocular problem but it is iatrogenic

Cornea: look for scratch with or without stain; epithelial erosion (punctate epithelial erosion) or corneal abrasion (missing epithelium); assess tear layer with blink and time how long tears last; look for dryness

Aqueous tear deficiency: ocular surface disorder; dry eye from insufficient tear production; associated with a lot of corneal staining or epithelial disruption and low tear lake; in young patient, ask about dry mouth because tear deficiency associated with Sjogren’s; in general with eye disorders, important to determine whether localized or related to systemic disorder; consider graft versus host disease

Limbus: area where bulbar conjunctiva meets cornea; epithelial limbal stem cells responsible for keeping corneal epithelium clear and their absence results in conjunctiva overgrowing cornea to cause limbal stem cell deficiency; common causes are chemical burn or trauma; medical emergency that requires immediate eye flushing until pH normalizes (use strips); if pH does not normalize, particulate matter may need to be removed from under eyelid using irrigation (have patient look down and flip lid); examine ocular surface to assess damage; limbal ischemia (whiteness around limbus) indicates damage to limbal stem cells and limbal stem cell deficiency likely; red limbus is good sign that enough cells present to respond to injury; start topical antibiotic to minimize infection risk; consider topical prednisolone to decrease inflammation; cover with bandage contact lens or amniotic membrane covered by contact lens to decrease inflammation and make more hospitable environment on ocular surface; may give oral vitamin C to help with wound healing and oral doxycycline to decrease MMP9 (matrix metallopeptidase 9) levels; follow patient closely to monitor for infection and evaluate healing; main prognostic factor for healing after chemical burn is whether residual limbal stem cells present to repopulate corneal epithelium; vision suffers without a clear cornea

Conjunctivitis: inflammation of palpebral conjunctiva; normal conjunctiva pink with underlying straight blood vessels; in conjunctivitis, lining replaced by bumps (follicular conjunctivitis) of aggregated lymphocytes, papillae (fibrovascular bundles with blood vessels), or scarring; papillae any size; acute (less than 6 weeks) or chronic

Acute follicular conjunctivitis (adenoviral conjunctivitis): 2-3 days of watery red eye; bumps on conjunctiva with few papillae; some strains cause very severe disease with pseudomembranes on inner lining that appear white and milky and stuck to palpebral conjunctiva, require peeling to prevent permanent scarring; preauricular node not necessary to diagnose; 2 weeks after infection resolves, some patients have immune response manifest as little dots under corneal epithelium (subepithelial infiltrates), which can be chronic; treat with topical steroids (responsive but may recur); dots affect vision and cause light sensitivity; disease affects younger patients and severe disease can cause residual scarring and prolonged subepithelial infiltrates; treat with artificial tears; very contagious; patients should not touch eye or share towels; wash sheets and towels; usually bilateral but avoid touching other eye if unilateral; patients should not go to work; if patient requires membrane removal, start topical corticosteroid; recognize when membrane peels necessary versus conservative therapy

Acute papillary conjunctivitis: most commonly associated with bacterial infection; generally self-limited because most bacteria unable to penetrate intact epithelium; differentiate from viral conjunctivitis by looking at reaction of conjunctiva (follicles more common with virus and papillae more common with bacteria) and secretion type (viral is serosanguinous and bacterial has pus)

Gonococcal conjunctivitis: presents as hyper-acute conjunctivitis; copious pus; if untreated, can penetrate intact corneal epithelium and progress to corneal ulcer and perforation; treat aggressively and treat partners for this and chlamydia

Chronic follicular conjunctivitis: months of scant discharge, itching, burning; inferior conjunctival bumps/follicles; differential diagnosis — chlamydia conjunctivitis (serotypes D through K, sexually transmitted disease) does not cause scarring or vision loss; molluscum contagiosum of eyelid, lymphoma, and chlamydia trachoma (serotypes A to C) also cause follicular conjunctivitis

Trachoma: presents as cicatricial conjunctivitis of upper eyelid outside US where endemic; scarring noted when lids are flipped; causes so much morbidity because we blink many times a day and is like sandpaper continually scratching cornea and limbal stem cells; limbal stem cell deficiency results when there is corneal scarring and loss of limbal stem cells; causes vision loss

Molluscum contagiosum: eyelids; sometimes underneath inferior eyelash line and missed; presence should cause consideration of immunosuppression like HIV (more commonly associated with CMV retinitis)

Herpetic (HSV 1) disease: acute follicular or papillary conjunctivitis with vesicles on eyelid; primary presentation is blepharoconjunctivitis; skin lesion may be very subtle (pimple that resolves and people do not realize it is herpes); HSV resides within trigeminal ganglion; reactivation leads to many possible presentations; classic lesion is epithelial defect shaped like a flower (dendrite); treat with topical or oral antivirals to shorten disease course from 10 to 14 days to 7 to 10 days to minimize scarring; after dendrite resolves, HSV can cause interstitial keratitis (inflammation and scarring in corneal stroma); can cause endothelial disease; endothelial cells are pump cells of cornea and when inflamed, corneal edema results; HSV can cause inflammation inside eye; inflammation in anterior chamber is anterior chamber uveitis or iritis; HSV can enter drainage system and elevate pressure; HSV can infect retina and cause retinitis; HSV should be in differential for any eye disease presentation

Varicella-zoster virus (VZV): higher risk of eye disease if involves V1 distribution of trigeminal nerve; eye disease appears 1 to 4 weeks after rash; need to monitor for 1 month for eye complications; 50% of patients with V1 zoster (forehead, eye, and tip of nose) eventually develop eye disease; eye disease can involve corneal changes like pseudodendrites (heaped up pieces of mucous and inflammatory cells stuck to eye); can cause inflammation of anterior segment (iritis) or retinitis (rarer but more morbid); advocate for vaccination for all patients; treat VZV with 10 to 14 days of valaciclovir 1 g three times a day; if chronic or recurrent, consider suppressive therapy with 1 g once per day; many eye sequelae caused by immune response; patients with anterior chamber inflammation (iritis) require prolonged low-dose topical corticosteroids

Allergic acute or chronic papillary conjunctivitis: seasonal allergies do not affect vision

Vernal conjunctivitis: large papillae on upper palpebral conjunctiva (like trachoma); papillae rub against cornea and cause shield ulcers and vision loss; more common in children; treat acutely with topical prednisolone; to prevent onset of vernal conjunctivitis, pretreat with antihistamine and mast-cell inhibitor; most kids outgrow but important to maintain vision; treat with antihistamines and mast cell inhibitors

Perennial allergies: atopic keratoconjunctivitis; T-cell mediated and treated with t-cell inhibitors (tacrolimus ointment or oral t-cell mediators like cyclosporine and tacrolimus)

Cicatricial conjunctivitis: scarring in eyelids; may result from severe adenoviral infection; consider mucous membrane pemphigoid in older patient with waxing and waning course; diagnose with biopsy and immunohistochemistry to look for positions of immunoglobulins and complement in basement membrane; subcategorize using antigen and staining pattern; this systemic disease requires systemic treatment to prevent blindness; often diagnosed by ophthalmologist or dentist

Conjunctival granulomas: due to sarcoidosis, lymphoma, or mucous membrane pemphigoid; can be easily biopsied

Episcleritis: bulbar injection without palpebral changes (if palpebral changes present, it’s conjunctivitis); usually due to ocular surface conditions like dry eye and blepharitis; worrisome if bilateral or persistent because can be associated with systemic inflammatory diseases; need to differentiate episcleritis (superficial vessel inflammation, not painful) from scleritis (involves deeper vessels, painful, and more serious); redness in episcleritis superficial (can see redness in linear blood vessels) vs scleritis has deeper redness with purple hue; redness is mobile in episcleritis (use a Q-Tip to test), immobile in scleritis; phenylephrine removes redness in episcleritis but not scleritis

Scleritis: 50% have underlying etiology; commonly associated with systemic autoimmune disease (rheumatoid arthritis, vasculitis, relapsing polychondritis); most common autoimmune comorbidity is rheumatoid arthritis (because rheumatoid arthritis very common; 33% of patients have scleritis); 50% of patients with vasculitis (especially granulomatosis with polyangiitis — formerly known as Wegener’s disease) have scleritis; examine joints and check complete blood count (CBC), comprehensive metabolic panel (CMP), inflammatory disease markers (c-ANCA [cytoplasmic antineutrophil cytoplasmic antibody}, p-ANCA [perinuclear antineutrophil cytoplasmic antibody]), chest x-ray, urinalysis to look for end-organ damage; in vasculitis, look for hematuria with red blood cell casts; rule out infection with immune response, especially syphilis, tuberculosis (TB), Lyme disease

Diffuse anterior scleritis: most common type; redness is in anterior component (can see it and it is flat)

Nodular scleritis: has nodules

Necrotizing scleritis: white component that indicates necrosis within the redness and is an emergency — eyeball is melting; results from bacterial, viral, or fungal infection, so cultures essential; may also result from severe inflammatory disorder (vasculitis); treat inflammatory cases with systemic immunosuppressive therapy (oral prednisone); for some forms of mild scleritis can use high-dose NSAIDs (non-steroidal anti-inflammatory drugs) (ibuprofen 800 mg TID or naproxen 500 mg BID); NSAIDs cannot be used in patients with necrotizing disease; treat patients with systemic immune issues like rheumatoid arthritis with oral prednisone

Posterior scleritis: occasional presentation; redness not visible but ultrasound shows inflamed, thickened, choroid and sclera on B-scan

Scleromalacia perforans: very rare; seen in patients with long-standing, untreated rheumatoid arthritis; rarely seen now with new disease modifying agents; presents as scleral melt without inflammation; can see blue underlying choroid because sclera melted slowly over time

Keratitis: inflammation of cornea

Corneal ulcer: most common; can be caused by bacteria, viruses, acanthamoebae, fungi; cannot always tell what is causing by inspection; need culture and targeted therapy; most bacterial, so start with broad-spectrum antibiotics, refine treatment based on culture results; for fungal ulcer, start with natamycin (only commercially available agent); if need another antifungal, compound amphotericin or voriconazole; acanthamoeba more severe and difficult to treat; often delayed diagnosis and no specific anti-acanthamoebal agent; use general toxins like PHMB (polyhexamethylene biguanide, a pool cleaner); not very comfortable; patients who wear soft contact lenses and come in contact with contaminated water (eg, pond water) at risk

Peripheral corneal ulcer (peripheral ulcerative keratitis): can result from infection or autoimmune disease (rheumatoid arthritis, vasculitis)

Other causes of corneal ulcer or abrasion: neurotrophic etiologies, diabetes, lesion to trigeminal system; patients with history of zoster have decreased sensation, so epithelium breaks down and does not re-heal; if only epithelium involved, is called corneal epithelial defect; neurotrophic ulcers involve stroma and epithelium

Work up for corneal ulcer: rule out infection; systemic work up; differentiate from corneal abrasions with fluorescein to stain abrasion; see if underlying infiltrate present to differentiate traumatic but not infected from infected abrasion needing antibiotics; treat with scaffolding for neurotrophic epithelium to heal with bandage contact lens or amniotic membrane for inflammation; use newly approved treatment nerve growth factor (very expensive) when neurotrophic corneal epithelium does not heal

Iritis: very hard to see white blood cells floating in anterior chamber (hallmark of iritis) without slit-lamp; certain features can be seen with penlight to suggest iritis, anterior segment inflammation, or history of anterior segment inflammation; posterior synechia is scarring of iris to lens, causes irregular pupil; irregular pupil indicates possible eye inflammation, but also can be caused by trauma; cornea can be hazy; keratic precipitates are small dots in innermost cornea (white blood cells stuck to cornea) that cause haziness, indicate anterior chamber inflammation

Differential diagnosis of acute anterior chamber inflammation: systemic inflammatory disease (most common is HLA-B27-associated); ask about ankylosing spondylitis, psoriasis, and inflammatory bowel disease symptoms; also caused by infections and other inflammations; limited work up with HLA-B27, syphilis testing, and chest x-ray looking for sarcoid; sarcoid presents with acute anterior segment inflammation, red eye and anterior segment cell or more insidiously with white eye, no symptoms, and cells on examination; HLA-B27 disease commonly presents with acute red eye, photophobia, and cells inside eye

Glaucoma:

Closed angle glaucoma: has red eye; patients have narrow angles between iris and cornea and pupil dilates; angle may shut and pressure increase rapidly (from 15 to 60 mm Hg); very painful; anterior chamber will be very shallow; pupil may be stuck and not very resposive (partially dilated); if no Tono-Pen or other way to check pressure, have patient close eyes and touch 2 fingers back and forth over eyeball to press down; if you cannot indent globe, pressure is very elevated; globe should feel like tip of nose; ophthalmic exam necessary if worried about closed angle glaucoma because long-term high pressure damages optic nerve and must be lowered as quickly as possible with drops and laser; more common in Asians

Open angle glaucoma: most common type; pressure too high for optic nerve; some people have nerve damage at pressures of 12 mm Hg, and others not until pressures of 25 mm Hg; normal pressure usually 12 to 21 mm Hg; nerve damage at lower pressures is normotensive glaucoma; nerve damage at higher pressure is traditional open angle glaucoma

Evaluation and treatment: pressure is only modifiable risk; goal to lower pressure with drops, laser, or surgery; genetic and environmental components; many patients have family history; more severe in blacks than whites

Differential for red eye: orbit is area behind globe; any orbital process around muscles or optic nerve can cause venous congestion, redness, and proptosis; causes are vascular abnormality, tumor, infectious infiltrate; thyroid eye; look for restricted eye movement, proptosis, redness; use imaging (ultrasonography, CT) to identify; cavernous carotid fistula after trauma

Emergency indicators: red eye with pain, vision loss, history of recent surgery, or eye looks funny

Dry eye: misnomer; in Sjogren’s, people actually have dry eyes because do not make enough tears, inflammation causes scratchiness of cornea and damaged epithelium, which is seen with fluorescein, often accompanied by dry mouth; most people who say their eyes feel dry do not have aqueous tear deficiency; a complaint of dry eye is an umbrella term for dry eye symptoms and signs; symptoms are generally sensations; patients complain about eyes feeling dry, burning, and aching and about visual quality; if vision is clear after blinking but becomes blurry until re-blinking, indicates unstable tear film; many different dry eye signs that can accompany these symptoms like inadequate tear production, fast tear evaporation, inflammation, high osmolarity

Aqueous tear deficiency: actual dryness; measure with strips of paper to measure tear production or use slit-lamp to look at tear lake; deficiency associated with Sjogren’s, graft versus host disease, and other autoimmune conditions

Meibomian gland dysfunction: contributing factors are age (both lacrimal and Meibomian gland production decline with age), rosacea or any skin condition; look for anatomical issues like conjunctivochalasis, glaucoma surgery, pterygium that impacts tear mixing on ocular surface; nerve dysfunction — some patients with fibromyalgia or other chronic pain conditions

Treatment: anti-inflammatory agents; T-cell inhibitors; topical cyclosporine; lifitegrast is a drug which inhibits integrin and lymphocyte function-associated antigen 1 (LFA 1) from binding to ICAM-1 (intercellular adhesion molecule 1); effect is to block T-cells; blocking T-cells is commonly used in patients with dry eye and inflammatory component (Sjogren’s or graft versus host disease); if symptoms of dryness driven by lid disease, improve Meibomian gland function with lid hygiene; heat Meibomian glands to unblock openings on eyelid margin; decrease inflammation and improve oil quality by giving antibiotics (doxycycline); lasers to improve Meibomian gland health; fix anatomy by trimming conjunctiva in case of conjunctivochalasis; remove pterygiums and fix eyelid issues like ectropion and entropion; tell patients to use over-the-counter artificial tears first and refer if persistent symptoms; change environmental conditions if happens with prolonged screen time (take breaks, use artificial tears periodically while at computer), add humidifier; refer if ineffective

Cataract: anterior chamber disorder; leading cause of blindness worldwide; cataract is a change in the lens; refractive surfaces of the eye are cornea (provides 40 diopters refractive power) and lens (provides 20 diopters refractive power), which work together to get light to retina to see clear image; lens is metabolically active and changes over time; when young, lens is blue and easy to see through; with age, color changes to yellowish-green-brown color and becomes more opalescent (less able to shine light through it); development of cataract does not necessitate surgery; anyone over age 50 has some sort of lens change; look for lens opacity that is visually significant; happens at different time for different people; a person may have minor lens change, but if they are a photographer, they really notice it; some have vision of 20/70 and they can no longer watch TV; let patient tell when vision significantly affected; rare traumatic emergencies with penetration of capsule requires urgent cataract removal; cataract surgery usually elective

Retinal Disorders

Macular degeneration: retinal disorder with genetic and environmental components; whites more commonly affected than blacks, who, if affected, tend to have variant form; macula is center part of retina that supplies central vision; look for changes like drusen (yellow deposits) and atrophy of choroid (layer under retina that supplies retina with nutrients); two forms; wet form has abnormal vessels growing into retina; dry form has no abnormal vessels; optical coherence tomography (OCT) provides cross-sectional view of retina and shows vessels as fluid spaces within and under retina; important to distinguish between forms because wet macular degeneration treated with periodic anti-vascular endothelial growth factor (VEGF) injections, whereas dry macular degeneration with moderate or severe drusen (size, how fluffy, how much atrophy) treated with AREDS (age-related eye disease studies) vitamin formulation (vitamin C and zinc); vitamins modestly reduce risk of progression to wet macular degeneration; patients’ vision should be monitored for conversion from dry to wet; better visual prognosis if anti-VEGF therapy started soon after conversion

Retinal detachment: three types; rhegmatogenous retinal detachment results from tear; exudative retinal detachment results from fluid underneath retina; traction-related detachment; most common form results from tear with vitreous fluid tracking underneath retina causing detachment; biggest risk factor is aging, which makes vitreous more liquid and pulls off retina at some points; called posterior vitreal detachment; causes sudden black dot floating in vision that represents condensed part of vitreous floating through more liquefied layers because no longer attached to retina; look for presence of retinal tears, which occur within 4 to 6 weeks of vitreous detachment due to persistent vitreous adhesions to retina that tear with movement; re-check within 4 to 6 weeks; risk for new tear decreases after that; a tear without much subretinal fluid can be treated with laser in clinic to tack down and prevent progression to retinal detachment; if tear missed and enough fluid goes underneath, need surgery; can wrap scleral buckle outside eye to compress area of tear and use cryotherapy, which was preferred approach; now more popular approach is repair of retina from inside using vitrectomy; in complex cases, use both; new onset floaters or flashes of light could indicate a retinal tear and require ophthalmologic evaluation

Retinal vein occlusion: acute vision loss; occurs in older patients with vascular risk (diabetes, hyperlipidemia, hypertension, smoking, metabolic syndromes) and those with raised intraocular pressure; sometimes associated with malignancy, hypercoagulable state; determine what systemic conditions contributing and reduce risk

Central retinal vein occlusion: dramatic presentation of disc swelling, tortuous veins, and heme throughout retina; if ischemic, patients at higher risk developing neovascularization of iris, which closes angle and causes neovascular glaucoma; very challenging to manage, so use laser on ischemic retinal area to decrease overall metabolic load and prevent vessel formation; another strategy is anti-VEGF injections if vessels form

Hemi-vein occlusion (HRVO) or branch retinal vein occlusion (BRVO): similar presentation of tortuous veins and heme in affected quadrant; much less likely to have neovascularization because less ischemia; main complication is macular edema (fluid accumulation in macula), which decreases vision; treat with anti-VEGF injections every 1 to 3 months; OCT very useful to screen for macular edema, but clinical exam crucial to evaluate for presence of iris neovascularization

Retinal artery occlusion: less common but similar risk factors to central retinal vein occlusion; embolic disease affects central retinal artery or branch; visual loss is more devastating in central retinal artery occlusion than central retinal vein occlusion; very small arteries with diffuse retinal whitening and cherry red spot; fovea appears red because contrasts with retinal swelling in surrounding retina; attempts to restore vision with eye massage to dislodge emboli or lower pressure, but nothing changes course or visual prognosis, which is guarded; main goal to treat systemic disease like diabetes, hyperlipidemia; consider giant cell arteritis or temporal arteritis as underlying etiologies

Endophthalmitis: infection within eye; exogenous endophthalmitis associated with recent eye surgery and pathogen introduced through surgical wound; endogenous endophthalmitis associated with systemic infection and need to find source; sample fluid from front part of eye or vitreous cavity; inject antibiotics into eye before waiting for confirmatory culture because faster control is better; after culture results, treat locally with intracameral or intravitreal antibiotics or antifungals; if severe, surgical cleaning of vitreous cavity to decrease burden of infectious organisms; prognosis guarded and depends on type of organism; Staphylococcus epidermidis after cataract surgery has better prognosis than Streptococcus species

Cellulitis: orbital cellulitis versus periorbital cellulitis; periorbital does not involve orbital septum and has much better prognosis; orbital cellulitis can affect optic nerve and cause visual loss; differentiate clinically and with imaging; patient with orbital cellulitis should be hospitalized and treated with intravenous antibiotics; periorbital cellulitis observed, treated with oral antibiotics; signs of orbital involvement include vision loss, optic nerve involvement (afferent pupillary defect), restriction of eye movement, proptosis; treat, monitor orbital more closely

Optic neuritis: inflammation of optic nerve; presentation is decreased vision with color vision loss, pain with eye movement; can be associated with multiple sclerosis (MS)

Anterior ischemic optic neuropathy (AION): acute vision loss; optic nerve slightly swollen; determine if associated with temporal arteritis, which makes vision loss worse; optic nerve is pale, chalky white; non-temporal arteritis-associated AION associated with diabetes, hypertension; vision loss may not be as severe and optic nerve does not look as bad; sectorially but not diffusely swollen, not chalky white; differentiate between arteritic process (associated with temporal arteritis) or non-arteritic process; look at optic nerve, determine if optic neuropathy and subtype

Trauma: should cause concern about globe, as in superficial lesions of corneal abrasion or conjunctival laceration (heal without intervention); fluorescein strip to see if epithelial disruption on ocular surface; worry about penetration of object into eye or laceration; trauma patients may have multiple issues and eye exam often delayed; look at eyeball, gently check if pressure low, which is a sign of laceration or penetration; see if anterior chamber is deep, iris is regular, pupil is regular; pupil irregularity with pulling to an area is a sign of penetration; look at white part of eye for bleeding associated with a hole in the eye; type of trauma increases or decreases risk; metal projectiles easily penetrate eye; small penetrations may be missed; if anterior segment looks funny, put shield over eye, do not let patient rub eye; low threshold for referral, especially if person was working with metal or says there was a high-impact foreign body that went toward the eye; if patient reports that a leaf or dirt fell into eye, penetration less likely; injuries involving plants (branch, thorn) may cause infections with fungi or bacteria; treat with antibiotics and follow closely

Uveitis: inflammation of uvea or any part of eye; anterior chamber uveitis/iritis includes scleritis; uveitis categorized by anatomical components that are inflamed; HLA-B27 disorders most commonly associated with iritis; 50% of patients with iritis have systemic association (40% are HLA-B27, sarcoidosis, syphilis)

Intermediate uveitis or vitreitis: inflammation mainly in vitreous cavity; differential includes infections (syphilis, TB, Lyme), inflammatory (MS, sarcoidosis), lymphoma, primary CNS lymphoma

Retinitis: inflammation of retina; typically infection with virus; CMV associated with immunosuppression in HIV; HSV and zoster very serious because retinitis can spread very quickly and cause vision loss; aggressively treat; Behcet’s disease less common cause of inflammatory retinitis; focal chorioretinitis is classic presentation of toxoplasmosis, associated dense vitreitis over lesion; treatment of infection plus oral corticosteroids 48 hours after starting anti-infective (double strength Bactrim twice a day to deal with inflammatory consequences of toxoplasmosis); choroiditis seen in multiple conditions (most commonly sarcoidosis); diseases of retina and choroid without systemic diagnosis such as multifocal choroiditis with panuveitis, in which the anterior chamber vitreous is inflamed and there are punched up choroidal lesions; determine if disease localized or systemic; treat inflammatory anterior uveitis with topical corticosteroids but may need local injections or systemic therapy if there is need to penetrate to vitreous or posterior part of eye or if systemic

Readings

Cronau H et al: Diagnosis and management of red eye in primary care. Am Fam Physician 2010 Jan;81(2):137-44; McGinnigle S et al: Evaluation of dry eye. Surv Ophthalmol 2012 Jul-Aug;57(4):293-316; Pflipsen M et al: Evaluation of the painful eye. Am Fam Physician 2016 Jun;93(12):991-8.

Disclosures

For this activity, the following has been disclosed: Dr. Galor is a consultant for Novaliq, Shire, Dompe, and Allergan. The planning committee reported nothing to disclose.

Acknowledgements

CME/CE INFO

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