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Conjunctival inflammation typically results from infection, allergy, or irritation. Symptoms are conjunctival hyperemia and ocular discharge and, depending on the etiology, discomfort and itching. Diagnosis is clinical; sometimes cultures are indicated. Treatment depends on etiology and may include topical antibiotics, antihistamines, mast cell stabilizers, and corticosteroids.
Infectious conjunctivitis is most commonly viral or bacterial and is contagious. Rarely, mixed or unidentifiable pathogens are present. Numerous allergens can cause allergic conjunctivitis (see Conjunctival and Scleral Disorders: Allergic Conjunctivitis). Nonallergic conjunctival irritation can result from foreign bodies; wind, dust, smoke, fumes, chemical vapors, and other types of air pollution; and intense ultraviolet light of electric arcs, sunlamps, and reflection from snow.
Conjunctivitis is typically acute, but both infectious and allergic conditions can be chronic. Conditions that cause chronic conjunctivitis include ectropion, entropion, blepharitis, and chronic dacryocystitis.
Symptoms and Signs
Any source of inflammation causes lacrimation or discharge and diffuse conjunctival vascular dilation. Discharge may cause the eyes to crust overnight. Thick discharge may blur vision, but once discharge is cleared, visual acuity should be unaffected.
Itching and watery discharge predominate in allergic conjunctivitis. Chemosis and papillary hyperplasia also suggest allergic conjunctivitis. Irritation or foreign body sensation, photophobia, and discharge suggest infectious conjunctivitis; purulent discharge suggests a bacterial cause. Severe eye pain suggests scleritis (see Conjunctival and Scleral Disorders: Scleritis).
Diagnosis
Usually, diagnosis is made by history and examination (see also Table 1: Conjunctival and Scleral Disorders: Differentiating Features in Acute Conjunctivitis ), usually including slit-lamp examination with fluorescein staining of the cornea and, if glaucoma is suspected, measurement of intraocular pressure.
Other disorders can cause a red eye (see Symptoms of Ophthalmologic Disorders: Red Eye). Deep pain in the affected eye when a light is shone in the unaffected eye (true photophobia) does not occur in uncomplicated conjunctivitis and suggests a disorder of the cornea or anterior uveal tract. Circumcorneal conjunctival hyperemia (sometimes described as ciliary flush) is caused by dilated, fine, straight, deep vessels that radiate out 1 to 3 mm from the limbus, without significant hyperemia of the bulbar and tarsal conjunctivae. Ciliary flush occurs with uveitis, acute glaucoma, and some types of keratitis.
The cause of conjunctivitis is suggested by clinical findings. However, cultures are indicated for patients with severe symptoms, immunocompromise, a vulnerable eye (eg, after a corneal transplant, in exophthalmos due to Graves' disease), or ineffective initial therapy.
Clinical differentiation between viral and bacterial infectious conjunctivitis is not highly accurate. However, temporarily missing some cases of mild bacterial conjunctivitis is not likely to be harmful because the infection often resolves spontaneously and antibiotics can be prescribed if symptoms persist.
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Table 1
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| Differentiating Features in Acute Conjunctivitis |
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Etiology
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Discharge/Cell Type
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Eyelid Edema
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Node Involvement
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Itching
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Bacterial
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Purulent/Polymorphonuclear leukocytes
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Moderate
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Usually none
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None
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Viral
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Clear/Mononuclear cells
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Minimal
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Usually
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None
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Allergic
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Clear, mucoid, ropy/Eosinophils
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Moderate to severe
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None
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Mild to intense
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Treatment
Most infectious conjunctivitis is highly contagious and spreads by droplet, fomites, and hand-to-eye inoculation. To avoid transmitting infection, physicians must wash their hands thoroughly and disinfect equipment after examining patients. Patients should wash their hands thoroughly after touching their eyes or nasal secretions, avoid touching the noninfected eye after touching the infected eye, avoid sharing towels or pillows, and avoid swimming in pools. Eyes should be kept free of discharge and should not be patched. Small children with conjunctivitis should be kept home from school to avoid spread. Cool washcloths applied to the eyes may help relieve local burning and itching. Antimicrobials are used for certain infections.
Viral Conjunctivitis
Viral conjunctivitis is a highly contagious acute conjunctival infection usually caused by adenovirus. Symptoms include irritation, photophobia, and watery discharge. Diagnosis is clinical. Infection is self-limited, but severe cases sometimes require topical corticosteroids.
Etiology
Conjunctivitis may accompany the common cold and other systemic viral infections (especially measles, but also chickenpox, rubella, and mumps). Isolated viral conjunctivitis usually results from adenoviruses and sometimes enteroviruses.
Epidemic keratoconjunctivitis usually results from adenovirus serotypes Ad 5, 8, 11, 13, 19, and 37. Pharyngoconjunctival fever usually results from serotypes Ad 3, 4, and 7. Outbreaks of acute hemorrhagic conjunctivitis, a rare conjunctivitis associated with infection by enterovirus type 70, have occurred in Africa and Asia.
Symptoms and Signs
After an incubation period of about 5 to 12 days, conjunctival hyperemia, watery discharge, and ocular irritation usually begin in one eye and spread rapidly to the other. Follicles may be present on the palpebral conjunctiva. A preauricular lymph node is often enlarged and painful. Many patients have had contact with someone with conjunctivitis, a recent URI, or both.
In severe adenoviral conjunctivitis, patients may have photophobia and foreign body sensation. Chemosis may be present. Pseudomembranes of fibrin and inflammatory cells on the tarsal conjunctiva, focal corneal inflammation, or both may blur vision. Even after conjunctivitis has resolved, residual corneal subepithelial opacities (multiple, coin-shaped, 0.5 to 1.0 mm in diameter) may be visible with a slit lamp for up to 2 yr. Corneal opacities occasionally result in decreased vision and significant glare.
Diagnosis
Diagnosis of conjunctivitis and differentiation between bacterial, viral, and noninfectious conjunctivitis are usually clinical; special tissue cultures are necessary for growth of the virus but are rarely indicated. Features that may help differentiate between viral and bacterial conjunctivitis can include purulence of eye discharge, presence of preauricular lymphadenopathy, and, in epidemic keratoconjunctivitis, chemosis. Patients with photophobia are stained with fluorescein and examined with a slit lamp. Epidemic keratoconjunctivitis may cause punctate corneal staining. Secondary bacterial infection of viral conjunctivitis is rare. However, if any signs suggest bacterial conjunctivitis (eg, purulent discharge), smears from the eye may be examined microscopically and cultured for bacteria.
Treatment
Viral conjunctivitis is highly contagious, and transmission precautions must be followed (as described previously). Children should generally be kept out of school until resolution.
Viral conjunctivitis is self-limiting, lasting 1 wk in mild cases to up to 3 wk in severe cases. It requires only warm or cool compresses for symptomatic relief. However, patients who have severe photophobia or whose vision is affected may benefit from topical corticosteroids (eg, 1% prednisolone acetate q 6 to 8 h). Corticosteroids, if prescribed, are usually prescribed by an ophthalmologist. Herpes simplex keratitis (see Corneal Disorders: Herpes Simplex Keratitis) must be ruled out first (by fluorescein staining and slit-lamp examination) because corticosteroids can exacerbate it.
Acute Bacterial Conjunctivitis
Acute conjunctivitis can be caused by numerous bacteria. Symptoms are hyperemia, lacrimation, irritation, and discharge. Diagnosis is clinical. Treatment is with topical antibiotics, augmented by systemic antibiotics in more serious cases.
Most bacterial conjunctivitis is acute; chronic bacterial conjunctivitis may be caused by Chlamydia and rarely Moraxella. Chlamydial conjunctivitis includes trachoma and adult or neonatal inclusion conjunctivitis.
Etiology
Bacterial conjunctivitis is usually caused by Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus sp, or, less commonly, Chlamydia trachomatis (see Conjunctival and Scleral Disorders: Adult Inclusion Conjunctivitis). Neisseria gonorrhoeae causes gonococcal conjunctivitis, which usually results from sexual contact with a person who has a genital infection.
Ophthalmia neonatorum (see also Infections in Neonates: Neonatal Conjunctivitis) is conjunctivitis that occurs in 20 to 40% of neonates delivered through an infected birth canal. It can be caused by maternal gonococcal or chlamydial infection.
Symptoms and Signs
Symptoms are typically unilateral but frequently spread to the opposite eye within a few days. Discharge is typically purulent.
The bulbar and tarsal conjunctivae are intensely hyperemic and edematous. Petechial subconjunctival hemorrhages, chemosis, photophobia, and an enlarged preauricular lymph node are typically absent. Eyelid edema is often moderate.
With adult gonococcal conjunctivitis, symptoms develop 12 to 48 h after exposure. Severe eyelid edema, chemosis, and a profuse purulent exudate are typical. Rare complications include corneal ulceration, abscess, perforation, panophthalmitis, and blindness.
Ophthalmia neonatorum caused by gonococcal infection appears 2 to 5 days after delivery. With ophthalmia neonatorum caused by a chlamydial infection, symptoms appear within 5 to 14 days. Symptoms of both are bilateral, intense papillary conjunctivitis with lid edema, chemosis, and mucopurulent discharge.
Diagnosis
Diagnosis of conjunctivitis and differentiation between bacterial, viral, and noninfectious conjunctivitis are usually clinical. Smears and bacterial cultures should be done in patients with severe symptoms, immunocompromise, ineffective initial therapy, or a vulnerable eye (eg, after a corneal transplant, in exophthalmos due to Graves' disease). Smears and conjunctival scrapings should be examined microscopically and stained with Gram stain to identify bacteria and stained with Giemsa stain to identify the characteristic epithelial cell basophilic cytoplasmic inclusion bodies of chlamydial conjunctivitis.
Treatment
Bacterial conjunctivitis is very contagious, and standard infection control measures (see Conjunctival and Scleral Disorders: Treatment) should be followed.
If neither gonococcal nor chlamydial infection is suspected, most clinicians treat presumptively with moxifloxacin 0.5% drops tid for 7 to 10 days or another fluoroquinolone or trimethoprim/polymyxin B qid. A poor clinical response after 2 or 3 days indicates that the cause is resistant bacteria, a virus, or an allergy. Culture and sensitivity studies determine subsequent treatment.
Adult gonococcal conjunctivitis requires a single dose of ceftriaxone 1 g IM. Fluoroquinolones are no longer recommended because resistance is now widespread. Bacitracin 500 U/g or gentamicin 0.3% ophthalmic ointment instilled into the affected eye q 2 h may be used in addition to systemic treatment. Sex partners should also be treated. Because chlamydial genital infection is often present in patients with gonorrhea, patients should also receive a single dose of azithromycin 1 g or doxycycline 100 mg po bid for 7 days.
Ophthalmia neonatorum is prevented by the routine use of silver nitrate eye drops or erythromycin ointment at birth. Infections that develop despite this treatment require systemic treatment. For gonococcal infection, ceftriaxone 25 to 50 mg/kg IV or IM is given once/day for 7 days. Chlamydial infection is treated with erythromycin 12.5 mg/kg po or IV qid for 14 days. The parents should also be treated.
Adult Inclusion Conjunctivitis
(Adult Chlamydial Conjunctivitis; Swimming Pool Conjunctivitis)
Adult inclusion conjunctivitis is caused by sexually transmitted Chlamydia trachomatis. Symptoms include chronic unilateral hyperemia and mucopurulent discharge. Diagnosis is clinical. Treatment is with systemic antibiotics.
Adult inclusion conjunctivitis is caused by Chlamydia trachomatis serotypes D through K. In most instances, adult inclusion conjunctivitis results from sexual contact with a person who has a genital infection. Usually, patients have acquired a new sex partner in the preceding 2 mo. Rarely, adult inclusion conjunctivitis is acquired from contaminated, incompletely chlorinated swimming pool water.
Symptoms and Signs
Adult inclusion conjunctivitis has an incubation period of 2 to 19 days. Most patients have a unilateral mucopurulent discharge. The tarsal conjunctiva is often more hyperemic than the bulbar conjunctiva. Characteristically, there is a marked tarsal follicular response. Occasionally, superior corneal opacities and vascularization occur. Preauricular lymph nodes may be swollen on the side of the involved eye. Often, symptoms have been present for many weeks or months and have not responded to topical antibiotics.
Diagnosis
Chronicity, mucopurulent discharge, marked tarsal follicular response, and failure of topical antibiotics differentiate adult inclusion conjunctivitis from other bacterial conjunctivitides. Smears, bacterial cultures, and chlamydial studies should be done. Immunofluorescent staining techniques, PCR, and special cultures are used to detect C. trachomatis. Smears and conjunctival scrapings should be examined microscopically and stained with Gram stain to identify bacteria and stained with Giemsa stain to identify the characteristic epithelial cell basophilic cytoplasmic inclusion bodies of chlamydial conjunctivitis.
Treatment
Azithromycin 1 g po once only or either doxycycline 100 mg po bid or erythromycin 500 mg po qid for 1 wk cures the conjunctivitis and concomitant genital infection. Sex partners also require treatment.
Allergic Conjunctivitis
(Atopic Conjunctivitis; Atopic Keratoconjunctivitis; Hay Fever Conjunctivitis; Perennial Allergic Conjunctivitis; Seasonal Allergic Conjunctivitis; Vernal Keratoconjunctivitis)
Allergic conjunctivitis is an acute, intermittent, or chronic conjunctival inflammation usually caused by airborne allergens. Symptoms include itching, lacrimation, discharge, and conjunctival hyperemia. Diagnosis is clinical. Treatment is with topical antihistamines and mast cell stabilizers.
Etiology
Allergic conjunctivitis is due to a type I hypersensitivity reaction to a specific antigen.
Seasonal allergic conjunctivitis (hay fever conjunctivitis) is caused by airborne pollen of trees, grasses, or weeds. It tends to peak during the spring, late summer, or early fall and disappear during the winter months—corresponding to the life cycle of the causative plant.
Perennial allergic conjunctivitis (atopic conjunctivitis, atopic keratoconjunctivitis) is caused by dust mites, animal dander, and other nonseasonal allergens. These allergens, particularly those in the home, tend to cause symptoms year-round.
Vernal keratoconjunctivitis is a more severe type of conjunctivitis most likely allergic in origin. It is most common among males aged 5 to 20 who also have eczema, asthma, or seasonal allergies. Vernal conjunctivitis typically reappears each spring and subsides in the fall and winter. Many children outgrow the condition by early adulthood.
Symptoms and Signs
General:
Patients report bilateral mild to intense ocular itching, conjunctival hyperemia, photosensitivity (photophobia in severe cases), eyelid edema, and watery or stringy discharge. Concomitant rhinitis is common. Many patients have other atopic diseases, such as eczema, allergic rhinitis, or asthma.
Findings characteristically include conjunctival edema and hyperemia and a discharge. The bulbar conjunctiva may appear translucent, bluish, and thickened. Chemosis and a characteristic boggy blepharedema of the lower eyelid are common. Chronic itching can lead to chronic eyelid rubbing, periocular hyperpigmentation, and dermatitis.
Seasonal and perennial conjunctivitis:
Fine papillae on the upper tarsal conjunctiva give it a velvety appearance. In more severe forms, larger tarsal conjunctival papillae, conjunctival scarring, corneal neovascularization, and corneal scarring with variable loss of visual acuity can occur.
Vernal keratoconjunctivitis:
Usually, the palpebral conjunctiva of the upper eyelid is involved, but the bulbar conjunctiva is sometimes affected. In the palpebral form, square, hard, flattened, closely packed, pale pink to grayish cobblestone papillae are present, chiefly in the upper tarsal conjunctiva. The uninvolved tarsal conjunctiva is milky white. In the bulbar (limbal) form, the circumcorneal conjunctiva becomes hypertrophied and grayish. Discharge may be tenacious and mucoid, containing numerous eosinophils.
Occasionally, a small, circumscribed loss of corneal epithelium occurs, causing pain and increased photophobia. Other corneal changes (eg, central plaques) and white limbal deposits of eosinophils (Trantas' dots) may be seen.
Diagnosis
The diagnosis is usually clinical. Eosinophils are present in conjunctival scrapings, which may be taken from the lower or upper tarsal conjunctiva; however, such testing is rarely indicated.
Treatment
Avoidance of known allergens and use of tear supplements can reduce symptoms; antigen desensitization is occasionally helpful. Topical OTC antihistamine/vasoconstrictors (eg, naphazoline/pheniramine) are useful for mild cases. If these drugs are insufficient, topical prescription antihistamines (eg, olopatadine, ketotifen), NSAIDs (eg, ketorolac), or mast cell stabilizers (eg, pemirolast, nedocromil, azelastine) can be used separately or in combination. Topical corticosteroids (eg, loteprednol, fluorometholone 0.1%, prednisolone acetate 0.12% to 1% drops tid) can be useful in recalcitrant cases. Because topical corticosteroids can exacerbate ocular herpes simplex virus infections, possibly leading to corneal ulceration and perforation and, with long-term use, to glaucoma and possibly cataracts, their use should be initiated and monitored by an ophthalmologist. Topical cyclosporine may be indicated when corticosteroids are needed but cannot be used.
Seasonal allergic conjunctivitis is less likely to require multiple drugs or intermittent topical corticosteroids.
Last full review/revision June 2008 by Mitchell H. Friedlaender, MD
Content last modified June 2008
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