Ocular Symptoms and Signs

Authors: Lucia Sobrin, M.D.Janet L. Davis, M.D.

Patients who present with acute eye complaints can be challenging to the non-ophthalmologists who care for them in the emergency room or primary care setting. This is true in part because most non-ophthalmologists have had limited training in eye disease and may not feel comfortable with even the basic slit lamp examination. This chapter will provide a framework for thinking about potential causes of eye complaints. It is not meant to be comprehensive but rather exposes the most common causes of various constellations of ocular symptoms and signs. Referral to an ophthalmologist may still be necessary in the majority of cases to definitively diagnose patients.


Subconjunctival Hemorrhage

Subconjunctival hemorrhage refers to bleeding from a superficial vessel. Most cases are spontaneous, with a higher incidence among patients who take aspirin or other anti-coagulants. Subconjunctival hemorrhage can also be a result of Valsalva maneuvers, such as forceful coughing, vomiting or straining. Trauma is another common cause of this finding. The majority of patients will not have any associated symptoms. They do not notice they have a red eye until they look in the mirror or someone else points it out to them. Examination reveals blood under the conjunctiva that is often limited to one sector of the eye. Blood pressure should be checked as there is an association with hypertension. A work-up for an abnormal coagulation is only required if the patient experiences recurrent episodes and has evidence of poor clotting elsewhere on physical exam. If the patient has a history of trauma, particularly with a sharp object, they should be referred for a thorough ophthalmic examination to rule out an occult rupture of the globe which could be hidden by the blood. In general, no treatment is required and the patient can be reassured that the hemorrhage will clear in one to two weeks.

Keratitis Sicca (Dry Eye Syndromes)

Dry eyes can also cause redness in the absence of other symptoms, although usually the patient will have other accompanying complaints such as foreign body sensation and eye discomfort. Most cases of dry eyes are idiopathic but the syndrome can be secondary to drugs such as antihistamines and collagen vascular disorders such Sjogren’s syndrome and rheumatoid arthritis. Idiopathic dry eye syndrome is seen most commonly among postmenopausal women, but can occur in patients of either sex at any age. Patients usually note that symptoms are exacerbated by prolonged eye use (e.g., computer work or reading) or windy, dry conditions. Slit lamp examination reveals a decreased tear meniscus and tear break up time. The diagnosis is confirmed with the Schirmer’s test. Filter paper is placed in the inferior conjunctival fornix of each eye for five minutes after topical anesthesia is placed (to decrease reflex tearing). Tears migrate down the filter paper for at least 10 mm for the test to be considered normal. Treatment for most patients consists of frequent artificial tear use. Lubricating ointment at night can be a useful adjunct. More severe cases may require punctual occlusion or topical cyclosporine. Patients need to understand that this is typically a chronic condition requiring ongoing therapy.


Blepharitis is a chronic staphylococcal infection of the eyelid margin. The most common associated symptoms are crusting around the eyes among awakening, itching and burning. Slit lamp examination shows red, thickened eyelid margins. Warm compresses several times a day and lid hygiene consisting of lid scrubbing of the eyelid margin with baby shampoo are usually sufficient to control symptoms. Erythromycin ointment can be helpful in severe cases. This is a chronic condition requiring therapy often for several weeks, if not months, at a time.

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Meibomian Gland Disease

Meibomian gland disease is an inflammation of the sebaceous glands that exit near the lash line. The malfunctioning of these glands leads to an unstable tear film. Meibomian gland disease is associated with rosacea and as such can be aggravated by environmental factors such as alcohol and coffee. Patients often will notice some burning and foreign body sensation along with chronic redness. Telangectasias along the eyelid margin and inspissated meibomian gland orifices are the usual findings on slit lamp exam. In severe cases, peripheral corneal neovascularization and infiltrates can develop. Treatment consists initially of warm compresses for the associated blepharitis, but often oral doxycycline therapy is required for complete symptoms suppression.


Episcleritis is most commonly idiopathic but is associated with collagen vascular disease in a minority of cases. Infectious causes are even more unusual but include herpes viruses, syphilis, and Lyme disease. Patients describe the acute onset of redness and mild pain, although a minority of patients has no discomfort. It is important to differentiate this entity from scleritis which has greater systemic implications. On slit lamp exam, one sees sectoral engorgement of vessels that run in a radial direction below the conjunctiva. In contrast with scleritis, the engorged vessels in episcleritis should blanch with application of 2.5% phenylephrine drops. Other differentiating features between episcleritis and scleritis are listed in Table 1. A work-up for collagen vascular diseases or infection should only be pursued if the review of systems or general physical examination suggests an underlying etiology. While topical steroid drops often relieve symptoms, rebound episcleritis can accompany the tapering of medication. Oral non-steroidal anti-inflammatory medications are a more definitive treatment. Episcleritis resolves within a few weeks but may be recurrent, and recurrent episodes may warrant exploration of underlying systemic disease.

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Infectious Conjunctivitis

Infectious conjunctivitis comes in two varieties: viral and bacterial (See Table 2). Viral conjunctivitis is more common and is typically adenoviral in etiology. Herpes simplex conjunctivitis is seen less frequently. The usual organisms implicated in bacterial conjunctivitis are Staphylococcus aureusStaphylococcus epidermidisStreptococcus pneumoniae, and Haemophilus influenza. An acute, hyperpurulent conjunctivitis is typically gonococcal. Chlamydia classically causes a chronic conjunctivitis.

Patients with conjunctivitis may have a clear history of recent contact with individuals who had red eyes. The viral variety can be accompanied by an upper respiratory infection or sore throat and typically begins in one eye and then involves the second eye a few days later. A history of awakening with eyelids stuck together is often elicited. General physical exam can reveal preauricular lymphadenopathy, especially with the viral variety. Slit lamp examination can help to distinguish between viral and bacterial causes. Conjunctival follicles see photos are more commonly seen with viruses while papillae are seen in bacterial conjunctivitis. There are exceptions to this rule, however, and often a mixed picture with both papillae and follicles can be seen. Clear, mucoid discharge is more indicative of a virus while purulent discharge is associated with bacteria. For herpetic disease, finding periocular vesicles is a key to the diagnosis.

Clear cases of viral conjunctivitis do not require a work-up, but if there is any doubt as to the diagnosis, cultures of ocular discharge are required. Viral disease is treated conservatively with artificial tears and cold compresses. It often takes one to two weeks for symptoms to resolve. If the patient describes loss of vision, he or she should be referred to an ophthalmologist to ensure they have not developed subepithelial corneal infiltrates that require topical steroid therapy. Cases of herpetic conjunctivitis can be treated with vidarabine ointment four to six times per day.

Therapy of bacterial conjunctivitis should be guided by culture results. In general topical antibiotics are given for seven days. Some specific medications that cover most pathogens are moxifloxacin, gatifloxacin and polymyxin B/trimethoprim drops four to six times per day. Bacitracin and erythromycin ointment four times per day will also be sufficient in most cases. A few bacterial etiologies will require systemic medication. If the history or gram stain is suggestive of gonococcal disease, one gram of intramuscular ceftriaxone should be given promptly. If chlamydial disease is present, oral doxycycline or azithromycin therapy are acceptable therapies. Haemophilus influenzae conjunctivitis requires oral amoxicillin/clavunalate because of potential for concomitant nonocular involvement. With more virulent cases, especially gonococcal disease, referral to an ophthalmologist to rule out corneal involvement is imperative. Bacterial conjunctivitis should resolve within days of starting appropriate antibiotic therapy.

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Allergic Conjunctivitis

Allergic conjunctivitis is common in patients with a history of seasonal allergies, atopy, and eczema. The most prominent symptom is itching. Both eyes are typically involved and have a watery discharge. Slit lamp exam shows conjunctival papillae which may be most prominent upon flipping the upper lid, especially in vernal disease. Collaboration with an allergist to identify causative allergens is necessary in severe or persistent cases. The best treatment is to eliminate the allergen. Many different topical anti-allergy regimens are effective, including olapatadine twice daily and cromolyn sodium four times daily. Fluoromethalone or another similar mild topical steroid is necessary for severe cases. Oral histamines are a good adjunctive treatment. Allergic conjunctivitis is a chronic condition that may require ongoing therapy with particular attention to prophylactic therapy prior to seasons when the disease tends to reactivate.


Dacryocystitis, inflammation of the lacrimal sac, is most often related to nasolacrimal duct obstruction. It is less commonly related to nasal surgery, trauma, lacrimal sac diverticulum, or sinus surgery. The typically-implicated organisms are staphylococci, streptococci, and diphteroids. Patients will complain of tearing, discharge and swelling over medial aspect of lower eyelid. Examination reveals red, tender edema over medial aspect of lower eyelid and discharge from the punctum when pressure is applied over the lacrimal sac. Any discharge expressed from the punctum should be cultured. Additionally, proptosis and restriction of ocular motility should be looked for as signs of progression to orbital cellulitis. Oral cephalexin, amoxicillin/clavunalate, ciprofloxacin or cefaclor for ten days are the typical antibiotic choices. If the patient is febrile or acutely ill, one should consider admission for intravenous antibiotics. In additional to systemic therapy, topical trimethoprim/polymyxin or moxifloxacin 4 times per day should be given. Dacrocystitis resolves within one to two weeks with appropriate oral antimicrobials. Cases that do not improve with medical treatment should be referred to an ophthalmologist for incision and drainage. Surgical correction of nasolacrimal duct obstruction is often needed to prevent recurrences even in cases that respond to antibiotics.


Canaliculitis, inflammation of the canaliculus which leads from the punctum to the lacrimal sac is caused most commonly by Actinomyces israeili and less commonly by Fusobacterium, Nocardia, and various fungi. Patients describe tearing, discharge and swelling over medial aspect of the upper or lower eyelid. The classic sign on slit lamp examination is a “pouting punctum,” swelling and erythema of the punctum in medial most aspect of eyelid margin. Discharge may be expressed from the punctum with pressure and should be cultured. These patients should be referred to an ophthalmologist as surgical removal of the obstructing secretions and irrigation with antifungal or antibacterial solution is often required and curative.

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Corneal Abrasions

Corneal abrasions are usually the result of either trauma or an anatomic corneal defect that causes recurrent erosions. The overwhelming majority of patients will describe trauma with a foreign object immediately before the onset of symptoms. Patient with recurrent erosion from inadequate adhesion of the corneal epithelium to the basement membrane typically describe onset of tearing, pain and foreign body sensation upon awakening. A corneal epithelial defect that stains with fluorescein see photos is the finding on slit lamp examination. Conjunctival injection and a swollen eyelid may also be present. It is important to evert the upper lid to ensure there is no retained subtarsal foreign body. Topical antibiotic should be given four times per day for one week. For non-contact lens wearers, erythromycin ointment or polymyxin B/trimethoprim is sufficient. Contact lens wearers need antipseudomonal coverage with ofloxacin or ciprofloxacin and should not use their lenses until the abrasion resolves. Patching is generally not recommended and is contraindicated in contact lens wearers. Rapidity of healing depends on the size of the abrasion, but generally most abrasions heal in two to three days.

Corneal Ulcers

Most corneal ulcers see photos are caused by bacteria. Fungal ulcers should be suspected in cases of corneal injury with plant material. Acanthamoeba is seen almost exclusively in contact lens wearers and herpes viruses cause corneal ulcers with distinctive features on examination which will be discussed below. Pain, redness, photophobia, and foreign body sensation are the usual symptoms. The physician should ask about contact lens use, swimming with contact lenses, trauma, and a foreign body to the eye. A white or yellowish-white infiltration of the cornea with fluorescein staining of the overlying epithelial defect is the key finding. Herpes viruses often have a dendrite like appearance to their epithelial defects.

An ophthalmologist should be consulted to obtain corneal cultures. If the patient is a contact lens wearer, their contact lens case and contact lens solution bottles should also be sent to the microbiology lab. The appropriate antibiotic therapy can range from polymyxin B/trimethoprim four times per day to fortified antibiotics every hour depending on the size and location of the bacterial ulcer. An ophthalmologist should make this determination. For fungal, Acanthamoeba and herpetic ulcer treatment, please see Table 3. Patients initially need daily follow-up to ensure the ulcer is improving and to rapidly implement the results of the cultures and sensitivities. If the ulcer is outside of the visual axis, recovery of vision is the norm. If the ulcer is in the visual axis, scarring may limit vision and corneal transplantation may be necessary for visual rehabilitation.

Anterior Uveitis

More than half of the cases of anterior uveitis are idiopathic. Blunt trauma can cause a self-limited form of the disease. Being HLA-B27 positive is most common systemic association among adults while juvenile idiopathic arthritis is more prevalent in children. Sarcoidosis and other systemic inflammatory conditions can be causative even when the systemic signs of the illness have not yet appeared. Tuberculosis, syphilis, and herpes simplex see photos are among the common infectious etiologies. Rifabutin and cidofovir are two drugs that can induce anterior uveitis.

Patients present with a painful red eye and photophobia. A review of systems to elicit history of associated systemic symptoms is crucial. Slit lamp examination needs to be performed to look for cell and flare in the anterior chamber. Keratic precipitates, white cell deposits on the corneal endothelium, are a suggestive finding. If the patient has a unilateral uveitis without any history of systemic symptoms, no work-up is needed. If the uveitis is bilateral or recurrent, a systemic work-up is indicated and should be directed by findings from the review of systems.

Topical steroid is the usual treatment with the frequency of application dependent on the severity of disease. Cycloplegic drops such as scopolamine 0.25% or atropine 1% will help with photophobia. Periocular steroid injections are needed in cases refractory to drop therapy. Oral steroid therapy is rarely needed; it is reserved for cases that are unresponsive to periocular steroid therapy. Of course, infectious causes should be treated with drops and the appropriate systemic antimicrobials. Most initial episodes of unilateral anterior uveitis resolve within one or two weeks. If uveitis is recurrent, it may necessitate chronic immunomodulatory therapy and underlying systemic disease processes must be addressed.


About half of the cases of scleritis are idiopathic. Connective tissue diseases, particularly rheumatoid arthritis, Wegener’s granulomatosis see photos, and relapsing polychondritis, are the most common systemic associations. Infections are a much less common cause: corneal ulcer pathogens can extend onto the sclera. Alternatively, some infections such as tuberculosis and Lyme disease can affect the sclera directly. Patients with scleritis describe severe, boring eye pain which often radiates to the forehead and head. This pain may keep them awake at night. Examination with natural light can reveal a bluish hue to the sclera along with dilation of blood vessels and redness. These dilated vessels do not blanch with 2.5% phenylephrine and do not move when the conjunctiva is moved with a cotton swab.

Testing for the systemic disorders, directed by findings on history and exam, should be done in all cases of scleritis. Oral NSAIDs may be sufficient in milder cases, but oral steroids are often needed in moderate to severe cases. Recurrent scleritis may need systemic immunomodulatory therapy. Infectious causes are treated with systemic antibiotics. Scleritis can be a chronic disease requiring long term therapy. Patients need to be monitored for scleral thinning in areas of previous inflammation.

Acute Angle-Closure Glaucoma

Patients with acute angle-closure glaucoma have a sudden onset of pain, blurred vision and halos around lights. They often have associated nausea, vomiting and headache. Increased intraocular pressure, a closed angle with a shallow anterior chamber, and corneal edema are the usual findings. These patients should be referred to an ophthalmologist for gonioscopy to confirm diagnosis. Treatment consists of intraocular pressure control with drops and laser peripheral iridectomy.

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Pterygia are caused by elastotic degeneration of the conjunctiva from exposure to sunlight and dry, windy conditions. They are most commonly located on the inner corner of the eye. When they become inflamed, they cause burning, irritation and redness. On examination, an inflamed pterygium is a red, wing-shaped fibrovascular tissue that extends onto the cornea. Aggressive lubrication with artificial tears can often relieve symptoms. Pterygia that are in the visual axis and impairing vision can be removed surgically. Inflammation can recur, and patients are advised to avoid dry, windy conditions that can exacerbate this.

Please see the sections on conjunctivitisdry eyes and blepharitis above.


Amaurosis Fugax

Amaurosis fugax is caused by an embolus, usually from the carotid artery. It can also result from atherosclerotic disease causing vascular insufficiency and ocular hypoperfusion with postural changes. Profound vision loss occurs in one eye and lasts seconds to minutes with vision returning to normal after episode. The ocular examination is usually normal. One may see an embolus in a retinal arteriole. The work-up should include a Doppler ultrasound of the carotid arteries and cardiac echocardiogram to look for an embolic source. The patient should also have an assessment for atherosclerosis risk factors including lipid levels, fasting blood glucose, and a HBA1C. If carotid narrowing is present, the physician should consider referral for evaluation of endarterectomy. A daily aspirin, control of atherosclerotic risk factors and smoking cessation are also important. If a patient has recurrence despite a negative work-up, a more thorough evaluation is necessary immediately. This disease can be a precursor to a central artery occlusion which almost always causes permanent, profound vision loss.

Ocular Migraine

Ocular migraine can cause a transient loss of vision and is not necessarily accompanied by headache and eye pain. The visual disturbance may be in the form of a visual field defect or flashes of light typical of a migraine aura. The ocular examination is usually normal. Brain imaging is indicated if migraines are atypical in any way, e.g. the visual disturbances persist. Treatment is with anti-migraine medications such as sumatriptan. Identification and avoidance of precipitating factors such as certain foods may help the patient substantially. Most patients can achieve good control of their disease by anticipating migraine episodes by early symptoms and treating themselves before symptoms progress.

Giant Cell Arteritis

Giant cell arteritis is an inflammation of medium sized arteries that affects primarily elderly, Caucasian patients. Patients can present early with headaches and vague visual complaints or later with sudden painless vision loss. They may have concurrent systemic symptoms including jaw claudication, weight loss, and temporal headaches. Palpation of temporal arteries for tenderness and enlargement is important. The possible ocular findings include ischemic optic neuropathy see photos (disc edema) or arterial occlusions. The patient may not have any exam findings if symptoms are transient. An immediate sedimentation rate and C-reactive protein are required. Temporal artery biopsy is needed in most cases to confirm the diagnosis. Immediate treatment with intravenous steroids followed by a slow taper of oral steroids over several months is usually necessary. Patients should have serial exams and ESRs during steroid taper to ensure no recurrence of inflammation. Clinicians need to maintain a high level of suspicion for this disease in elderly patients with headaches and vague eye complaints because when the disease progresses it can cause rapid, profound, and irreversible vision loss.

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Vitreous Hemorrhage

The common causes of vitreous hemorrhage see photos are posterior vitreous detachment, retinal tear, retinal detachment, and diabetic retinopathy. Concomitant flashes of light are more suggestive of vitreous detachment or retinal detachment/tear as the underlying etiology. Dilated examination is most helpful but the view to the fundus may be limited to varying degrees by the hemorrhage. If there is no view to fundus, an ultrasound is needed to rule out a retinal detachment. A fasting blood glucose and HBA1C should be done to rule out diabetes. If retinal detachment is not present, no intervention is done initially; vitreous hemorrhage most often clears within 2-3 months. If vitreous hemorrhage persists or if there is an associated retinal detachment, vitrectomy is recommended.

Retinal Detachment

Retinal detachment see photos secondary to retinal tears or breaks is more common in nearsighted patients and patients who have had cataract surgery or ocular trauma. Tractional retinal detachments can occur in diabetes. Patients with retinitis (acute retinal necrosis or CMV retinitis) are at high risk of developing this complication as well. Serous retinal detachments can occur with hypertension, pregnancy and certain autoimmune vasculopathies such as lupus. Typical symptoms are loss of vision, flashes of light, floaters, a dark curtain covering part of visual field. Diagnosis requires referral to a retinal specialist for a dilated exam. For the typical rhegmatogenous retinal detachment (a retinal detachment caused by a tear in the retina), no work up is necessary. Most diabetics that develop a tractional detachment have had a known history of diabetes and diabetic retinopathy before they progress to this late stage. Serous detachments require a blood pressure check and screening for autoimmune vasculopathies. Surgical repair is necessary for rhegmatogenous and tractional detachments, while treatment of underlying conditions usually sufficient for serous detachments.

Central Retinal Artery Occlusion

Central retinal artery occlusion is caused by an embolus, usually from the carotid artery or heart. It can also be a complication of giant cell arteritis (see above) or collagen vascular diseases such as systemic lupus erythematosus. Patients describe painless, sudden, profound vision loss in one eye that is often noticed on waking up in the morning. Fundus examination reveals a cherry red spot in center of macula with surrounding whitening (ischemia) of the retina  see photos. An afferent papillary defect is often present. The embolus itself is often not visible. As for amaurosis fugax patient, central artery occlusion patients require a Doppler ultrasound of the carotid arteries and cardiac echocardiogram to look for an embolic source. If giant cell arteritis is suspected, an ESR and CRP must be obtained immediately. Blood tests looking for atherosclerosis risk factors (lipid levels, fasting blood glucose, HBA1C) may also be useful. No treatment has proven effective for central retinal artery occlusions. Only treatments instituted within 1.5 hours of the onset of the occlusion have had anecdotal success. These include ocular massage (to dislodge the embolus), anterior chamber paracentesis, and intraocular pressure lowering medications. A daily aspirin, control of atherosclerotic risk factors and smoking cessation are important for preventing an occlusion from occurring in the contralateral eye. Vision usually does not recover, but patients need to be monitored closely initially for development of neovascularization.

Central Retinal Vein Occlusion

Central retinal vein occlusion is most associated with atherosclerosis or hypercoagulable states can lead to thrombosis. Less commonly, it can be a consequence of a vasculitis from infectious causes (e.g. syphilis) or autoimmune causes (e.g. systemic lupus erythematosus). Patients describe unilateral painless loss of vision. Fundus examination shows tortuous, engorged retinal venules see photos and four quadrants of intraretinal hemorrhages. The patient should be investigated for atherosclerotic risk factors. In younger patients without atherosclerotic risk factors, a hypercoagulability panel should be done. A daily aspirin as well as control of atherosclerotic risk factors or hypercoagulable states is crucial to prevent involvement of the contralateral eye. There are also new anti-vascular endothelial growth factor compounds that may help patients recover vision from macular edema, a common complication of vein occlusions. Patients need to be examined every month for the first three months after diagnosis - when they are at highest risk for neovascularization, a complication which requires prompt laser treatment. The visual prognosis is variable and depends most on the extent of ischemia and macular edema.

Ischemic Anterior Optic Neuropathy

Diabetes, hypertension, and elevated lipids are risk factors for ischemic anterior optic neuropathy. (See photograph under Giant Cell Arteritis.) Relative nocturnal hypotension may also play a role, particularly in patients on antihypertensive medications. Patients will describe sudden, painless loss of vision in one eye. They may have a second decrease in visual acuity or visual field in the same eye a few days after the initial symptoms. Pale disc swelling will be present; it often only involves a segment of the disc. An afferent pupillary defect and visual field defect are other signs of the disease. The most important aspect of the work-up is to rule out giant cell arteritis as the cause of the ischemic optic neuropathy by getting an ESR and CRP. The patient should also have an evaluation for hypertension, diabetes and hyperlipidemia and avoid taking antihypertensive medications at bedtime to avoid possible nocturnal hypotension. Daily aspirin has not been proven to be beneficial but is recommended by some. Almost half of patients will have some spontaneous improvement in the six months after the onset of symptoms.

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Optic Neuritis

Optic neuritis can have many etiologies but is most frequently associated with multiple sclerosis. Infectious cases are typically associated with viral infections such as herpes zoster or childhood infections such as measles. If there is granulomatous inflammation present, sarcoidosis and tuberculosis should be in the differential diagnosis. The loss of vision gradually occurs over hours to days and is associated with pain on eye movement and reduced color vision. The patient may notice associated neurologic symptoms, worsening of symptoms with increased body temperature (Uhthoff’s phenomenon), or altered perception of moving objects (Pulfrich’s phenomenon) if it is secondary to multiple sclerosis. Patients will usually have an afferent pupillary defect, visual field defect, and reduced color vision. Only one third of patients will have a swollen disc; two-thirds have retrobulbar optic neuritis. MRI of the brain and orbits with gadolinium should be done to rule out demyelinating disease. For cases that are not typical for MS, search for inflammatory and infectious etiologies by ordering appropriate tests such as ACE, RPR, FTA-Abs, and ESR. The patient’s blood pressure should be checked to ensure there is no hypertensive urgency leading to papilledema. If MRI reveals any demyelination, the patient should receive intravenous methylprednisolone 1g/day for three days followed by prednisone 1 mg/kg/day for 11 days with subsequent taper. Evidence of MS should also prompt referral to a neurologist for treatment with interferon beta. In general, vision recovers substantially with optic neuritis secondary to MS. The clinician should treat other inflammatory and infectious etiologies with the appropriate, respective medications.

Please see also anterior uveitis and acute angle closure glaucoma above.

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Preseptal and Orbital Cellulitis

Preseptal and orbital cellulitis can occur from spread of contiguous infection in the sinuses or lacrimal sac or from traumatic introduction of infection via puncture wound. The most common organisms are Staphylococcus aureus and streptococci species. The patient should be asked about a history of sinusitis, skin abrasions or insect bites. Examination reveals eyelid edema and erythema. The signs that indicate orbital cellulitis (spread of infection posterior to orbital septum) are pain with eye movement, restriction of ocular motility, proptosis, and optic neuropathy with afferent papillary defect. A CT scan of brain, orbits and sinuses should be obtained if there is any suspicion of orbital cellulitis, subperiosteal abscess, intraorbital foreign body, or tumor. Any open wound or area of drainage should be cultured although there is typically no site to culture. Blood cultures are indicated if there is a fever or other sign of systemic infection.

For most cases of preseptal cellulitis, a ten-day course of oral antibiotics such as amoxicillin/clavunalate or cefaclor is sufficient. For cases of severe preseptal cellulitis where the patient is systemically ill or cases of orbital cellulitis, intravenous antibiotics such as ampicillin/sulfbactam or ceftriaxone are necessary until patient shows improvement. If a subperiosteal abscess is discovered on CT scan, surgical drainage is needed. Surgical drainage of the sinuses may be required after the acute infection is controlled.

Most patients with preseptal cellulitis improve quickly on antibiotics. Patients with orbital cellulitis need to be monitored daily to ensure steady improvement. Any worsening of symptoms should prompt a CT scan to look for formation of a periosteal abscess.

Herpes Zoster Ophthalmicus

Herpes zoster ophthalmicus is caused by reactivation of virus, often in the setting of immunocompromise although it may occur in immunocompetent individuals. Patients classically have a vesicular rash in the distribution of the ophthalmic division of the trigeminal nerve on one side of the face. Careful examination of the cornea and retina is necessary to rule out ocular involvement. An HIV test should be done if there is any suspicion for AIDS. Please see Table 3 for specific treatment recommendations. Herpes zoster usually responds promptly to appropriate antiviral therapy; scarring may results in area of the lesions.


Chalazion (or stye) is the result of a blocked meibomian gland orifice; patients with blepharitis and rosacea are at higher risk for this condition. Patients describe an eyelid lump and erythema with spontaneous drainage in some cases. On examination, there is a subcutaneous nodule in eyelid with surrounding erythema and edema. The nodule may come to a point where yellow material is seen just beneath the skin. The patient should be referred to an ophthalmologist if there is any question that the nodule may represent something other than a chalazion. Warm compresses three times per day for ten minutes each time will lead to drainage and resolution in the great majority of cases. If warm compresses do not lead to resolution after one month, referral to an ophthalmologist is required for incision and drainage. In cases of recurrent chalazia, treatment of underlying, predisposing conditions such as meibomian gland disease may be necessary.

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Idiopathic Orbital Inflammation

Conditions such as Wegener’s granulomatosis, sarcoidosis and lymphoma can cause orbital inflammation and must be differentiated from idiopathic orbital inflammation (orbital pseudotumor). Noninfectious causes of orbital inflammation present in a similar way as orbital cellulitis with eyelid redness and edema, proptosis, and ocular motility restriction. The history may help point the diagnosis towards non-infectious causes if there is no evidence of sinusitis, trauma or insect bite. Lacrimal gland involvement is more common in idiopathic orbital inflammation.

A thickened posterior sclera, lacrimal gland involvement, and thickening of extraocular muscles including their tendons are all CT scan signs more consistent with idiopathic orbital inflammation. Blood tests to rule out other causes of orbital inflammation such as an ACE and ANCA should be drawn if there is reason to suspect them on examination or CT scan. Idiopathic orbital inflammation responds quickly to high dose prednisone. If there is a good response to initial steroids, the dose can be slowly tapered over several months. In cases where patients are unable to taper off prednisone without recurrence of disease, radiation or alternative immunomodulatory therapy such as mycophenolate mofetil may be indicated. If the diagnosis is uncertain, the response to steroid therapy is poor, or the case is atypical for idiopathic orbital inflammation, orbital biopsy should be done.

Allergic or Contact Dermatitis

Allergic or contact dermatitis can be caused by eye drops, cosmetics or facial creams. Patients will describe sudden onset of eyelid swelling that may be accompanied by a rash and periorbital itching. On examination, conjunctival chemosis can be prominent. Efforts should be made identify the causative agent if it is not readily apparent. Oral anti-histamines and cold compresses are helpful and the swelling usually resolves quickly, within days. Please also see the sections on blepharitis and conjunctivitis above.

Flashes of Light

Please see the sections on retinal detachmentposterior vitreous detachment, and migraine above.

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Corneal or Conjunctival Foreign Body

Corneal or conjunctival foreign bodies usually are acquired when no protective eyewear is used during activities such as automobile and construction work. The slit lamp is often necessary to identify the foreign body on cornea or conjunctiva. The upper eyelid must be flipped and inspected to rule out a subtarsal foreign body. A detailed examination should be performed by an ophthalmologist to ensure that there is no full thickness laceration of the eye that could indicate an intraocular foreign body. A CT scan should be obtained if there is any suspicion for an intraorbital or intraocular foreign body.

The foreign body can usually be removed at the slit lamp. Sometimes irrigation and sweeping of the fornices with a Q-tip is necessary if very small particulate matter is involved. After corneal foreign body removal, a corneal abrasion remains which must be followed closely to ensure no infection develops; a topical antibiotic is often used while the abrasion heals. Rapidity of healing depends on the size of the corneal abrasion.

Please see the sections on conjunctivitisdry eyes and blepharitis above.

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Giant Papillary Conjunctivitis

Giant papillary conjunctivitis is a consequence of accumulation of deposits on contact lenses from inadequate cleaning or overuse. The patient will note increased lens awareness and intolerance, mucous discharge, and itching. The upper eyelid must be everted to observe the giant papillae, and deposits on the contact lens can be seen at the slit lamp. Therapy involves a topical mast cell stabilizer and suspension of contact lens wear initially. Once the conjunctivitis resolves and the patient is ready to restart contact lens use, it is best to change to daily disposable soft lenses or rigid gas-permeable lenses. Most cases improve within a few weeks but more severe cases may persist for several months and require prolonged topical steroid use.

Please see the sections on allergic conjunctivitisdry eyes and blepharitis above.


Please see the sections on corneal ulcercorneal abrasionanterior uveitis and migraine.

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Posterior Uveitis

The most common causes of posterior uveitis include toxoplasmosis, sarcoidosis, and syphilis. Less common etiologies include histoplasmosis, Behcet’s disease, cat scratch disease, Lyme disease, toxocariasis, Vogt-Koyanagi-Harada syndrome, and lymphoma. In immunocompromised individuals, the following diseases should be in the differential diagnosis: CMV retinitis, Candida endophthalmitis, herpetic retinitis (acute retinal necrosis), endogenous endophthalmitis, and pneumocystis choroiditis. Immune-recovery uveitis is an entity specific to HIV patients with a history of CMV retinitis.

Blurred vision and floaters with occasional redness and pain see photos are the typical symptoms with this condition. It is important to solicit risk factors for immunosuppression as well as a history of foreign travel, pet exposure, and other systemic symptoms from the patient. Examination shows cells and haze in the vitreous see photos. Retinal or choroidal inflammatory lesions and retinal vasculitis may be present depending on the etiology. These patients should be referred to an ophthalmologist. Blood tests are obtained depending on the suspected diagnoses, and blood cultures may be helpful when infectious etiologies are possible. Vitrectomy with removal of vitreous for analysis may be necessary if the diagnosis is unclear from the blood tests and clinical picture. Chest imaging may also be necessary in the work-up for tuberculosis and sarcoidosis. Brain imaging is necessary in an immunocompromised patient with toxoplasmosis to rule out CNS involvement. Treatment depends on the underlying etiology; please see Tables 3 and 4 for treatment by diagnosis.

Please also see the sections on posterior vitreous detachment, posterior vitreous hemorrhage, and retinal detachment above.

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Nasolacrimal Duct Obstruction

In infants, nasolacrimal duct obstruction is the result of an imperforate membrane at the distal end of the nasolacrimal duct. In adults, it may be secondary to trauma or scarring from infectious dacryocystitis. It causes wet-looking eyes or frankly overflowing tears. On examination, reflux of mucopurulent or mucoid material from the punctum may be seen when pressure was applied to the lacrimal sac. In congenital cases, digital pressure to the canalicular system twice daily will lead to resolution in the majority of cases within one year. Erythromycin ointment should be used if there is mucopurulent discharge. In adults, surgery is often indicated. If signs of acute dacryocystitis develop, oral antibiotics are necessary.

Please see the sections on allergic conjunctivitiscorneal ulcerinfectious conjunctivitiscorneal abrasioncorneal or conjunctival foreign body, and dry eye syndrome.

Orbital Pain

Please see the sections on idiopathic orbital inflammationoptic neuritispreseptal and orbital cellulitis, and dry eye syndrome.

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1. Carroll SC, Gaskin BJ, Danesh-Meyer HV. Giant cell arteritis. Clin Experiment Ophthalmol 2006;34:159-73; quiz 94. [PubMed]

2. Givner LB. Periorbital versus orbital cellulitis. Pediatr Infect Dis J 2002;21:1157-8.[PubMed]

3. Katz B, Trobe JD, Beck RW. The optic neuritis treatment trial: implications for clinicians. Semin Ophthalmol 1995;10:214-20.[PubMed]

4. Lynn WA, Lightman S. The eye in systemic infection. Lancet 2004;364:1439-50.[PubMed]

5. Margo CE, Harman LE. Posterior vitreous detachment. How to approach sudden-onset floaters and flashing lights. Postgrad Med 2005;117:37-42. [PubMed]

6. Moraes HV, Jr. Ocular manifestations of HIV/AIDS. Curr Opin Ophthalmol 2002;13:397-403. [PubMed]

7. Opstelten W, Zaal MJ. Managing ophthalmic herpes zoster in primary care. Bmj 2005;331:147-51.[PubMed]

8.  Peate WF. Work-related eye injuries and illnesses. Am Fam Physician 2007;75:1017-22. [PubMed]

9.  Singh RP, Young LH. Diagnostic tests for posterior segment inflammation. Int Ophthalmol Clin 2006;46:195-208.[PubMed]

10. Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database Syst Rev 2006:CD004764. [PubMed]

11. Wirbelauer C. Management of the red eye for the primary care physician. Am J Med 2006;119:302-6.[PubMed]

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Table 1. Episcleritis vs. Scleritis





More commonly sectoral

Can be sectoral or diffuse


None or mild

Deep, severe, boring

Change with 2.5% phenylephrine

Injected vessels blanch

Injected vessels do not blanch

Qtip test

Injected vessels can be moved with a Q tip

Injected vessels cannot be moved with a Q tip

Table 2. Viral vs. Bacterial Conjunctivitis


Viral Conjunctivitis

Bacterial Conjuncitivitis


Watery, mucous


Conjunctival pathology



Preauricular adenopathy





Less Common

Table 3.  Treatment of Selected Ocular Diseases



Fungal corneal ulcers

Natamycin 5% drops or Amphotericin B 0.15% drops initially every 1 -2 hours with a slow taper over weeks once infection is controlled.  Topical steroids should be avoided.  Consider adding oral fluconazole or voricanazole in severe cases.

Acanthamoeba corneal ulcers

Polyhexamethyl biguanide 0.02%, Chlorhexidine 0.02%, or Propamidine isethionate 0.1% drops every hour.  Discontinue contact lens wear.

Herpes Simplex epithelial keratitis

Trifluorothymidine 1% drops 9 times per day with tapering as lesions heal over 14 days; subsequent prophylaxis with oral acyclovir 400 mg BID

Herpes Zoster ophthalmicus

Intravenous acyclovir 30 mg/kg/day in 3 doses, for 7 – 10 days in severely immuncompromised individuals.  Famiciclovir 500mg PO TID or Valacyclovir 1g TID in immunocompetent patients or reliable, immunocompromised patients with less severe disease.  Bacitracin ointment to skin lesions.

Immune-recovery uveitis associated with healed CMV retinitis

Topical prednisolone acetate with frequency depending on severity. Periocular steroid injection for visually symptomatic cystoid macular edema or vitritis. Avoid intravitreal injection of triamcinolone acetonide.

Necrotizing herpetic retinitis

Intravenous acyclovir 1,500 mg/m2 of body surface area in three divided doses for 7 – 10 days (associated with high rate of failure); consider addition of foscarnet to improve efficacy.

Intravenous foscarnet and/or ganciclovir if no response to acyclovir, or patient judged to be severely immunocompromised; complete induction courses of both drugs, then place on maintenance therapy with oral valacyclovir or valganciclovir.

Adjunctive local therapy for severe disease: Intravitreal injections of ganciclovir 2.0 mg and/or foscarnet 1.2 to 2.4 mg three times per week for two weeks, then once or twice per week until lesions healed

Toxoplasmosis chorioretinitis

Oral pyrimethamine 200 mg load then 25 mg BID, sulfadiazine 2 g load then 1 g QID, clindamycin 300 mg QID, folinic acid 10 mg twice weekly or 5 mg daily, for 4 to 6 weeks.

Alternatives: 1) Oral trimethoprim-sulfamethoxazole DS plus clindamycin 300 mg QID for 4 to 6 weeks. 2) Oral atovaquone 750 mg TID, clarithromycin 500 mg BID for 4 to 6 weeks (sulfa-intolerant patients or those who are uncontrolled on clindamycin or clindamycin plus pyrimethamine).

Pneumocystis choroiditis

Intravenous trimethoprim (5 mg/kg)/ sulfamethaxazole (25 mg/kg) Q 8 hours for 3 weeks or intravenous pentamidine 4 mg/kg daily.

Syphilitic chorioretinitis

Intravenous aqueous penicillin G 24 million units per day for ten days.  Alternative: intramuscular procaine penicillin G 2.4 million units per day for ten days; must be given with oral probenecid 500 mg QID. Intravenous treatment preferred in HIV infection.

Tuberculous choroiditis

Oral isoniazid 300 mg daily, rifampin 300 mg BID, ethambutol 15 mg/kg daily, or other three or four drug regimen.

Bartonella retinitis

Oral doxycycline 100 mg BID and rifampin 300 mg BID for 4 - 6 weeks.

Bacterial endophthalmitis

Intravitreal injection of vancomycin 1 mg and ceftazidime 2.25 mg. Treatment of underlying infection if endogenous endophthalmitis.

Fungal endophthalmitis

Local: Intravitreal injection of amphotericin 5 micrograms or voriconazole 100 micrograms usually at the time of pars plana vitrectomy to clear vitreous fungal colonies.

Systemic: Oral fluconazole 200 to 400 mg daily or intravenous amphotericin in escalating doses. Alternative:  voriconazole 200 mg PO BID

Intraocular lymphoma

High-dose intravenous methotrexate with or without radiation therapy.

Intrathecal chemotherapy for CNS involvement.

Salvage therapy with intravitreal injection of methotrexate 400 micrograms weekly X 4, then monthly for one year, for sight-threatening disease.

Table 4.  Treatment of CMV Retinitis: Dosing and Toxicities







Ganciclovir, Intravenous


5 mg/kg IV BID for 2-3 weeks


5 mg/kg IV daily


CBC, creatinine

Hematologic toxicity.  Dosage adjustment for reduced creatinine clearance.

Ganciclovir Intraocular Device

May be used for induction.  Releases 1.4 µg/hour.

Drug delivery lasts for 6-8 months. 

Ocular exams

Systemic antiviral often used perioperatively and during maintenance

Valganciclovir, Systemic

900 mg PO BID for 3 weeks

900 mg PO daily

CBC, creatinine

Hematologic toxicity.  Dosage adjustment for reduced creatinine clearance.

Foscarnet, Systemic

60 mg/kg IV TID or 90 mg/kg BID for 2-3 weeks

90 – 120 mg/kg IV daily

Creatinine, BUN, Ca++, Mg++

Nephrotoxicity, electrolyte imbalance

Cidofovir, Systemic

5 mg/kg IV Q week X 2 weeks

3-5 mg/kg IV Q 2 weeks

Creatinine, BUN, CBC

Nephrotoxicity, hematologic toxicity, uveitis.  Pre- and post-infusion probenecid 500 mg PO QID.

Ganciclovir, Intraocular Injection

200 to 2000 µg/0.1 mL 2 – 3 times per week for 2 –3 weeks

200-2000 µg/0.1 mL one time per week

Ocular exams

Off-label use

Foscarnet, Intraocular Injection

1.2 to 2.4 mg/0.1 mL 2 – 3 times per week

1.2 – 2.4 mg/.05 or .1 mL 1 time per week

Ocular exams

Off-label use

What's New

Fan NW, et al.  Hot Spring Hazards-Microsporidial Keratitis. In the Literature Section, Clin Infect Dis 2012;55:iii.

Bremond-Gignac D, Mariani-Kurkdjian P, et al. Efficacy and Safety of Azithromycin 1.5% Eye Drops for Purulent Bacterial Conjunctivitis in Pediatric Patients. Pediatr Infect Dis J. 2009 Nov 20. [Epub ahead of print]

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Review Article: Javey G, Zuravleff J.  Keratitis, 2007.

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