The red eye: diagnosis and treatment

Author: Jimmy H. Hara
Date: Dec, 1996

The red eye has various underlying etiologies and is usually benign (Table 1).[1] Causes that are not vision-threatening include subconjunctival hemorrhage, stye, chalazion, blepharitis, conjunctivitis, dry eyes and superficial corneal abrasions. Vision-threatening causes include orbital cellulitis, keratitis, uveitis, episcleritis/scleritis and acute primary angle-closure glaucoma. Keratopathy, uveitis and episcleritis/scleritis are frequently associated with circumcorneal injection or the so-called ciliary flush.

TABLE 1Symptoms as a Clue to Cause of Red EyeSymptom Possible causeItching Allergic conjunctivitisScratchy sensation Dry eyes, foreign body in the eye, blepharitisBurning Lid, conjunctival or corneal disordersLocalized lump Hordeolum (stye), chalazionor tenderness Iritis, keratopathy, glaucoma,Ocular pain scleritis, periorbital cellulitis, corneal abrasionsPhotophobia Iritis, keratopathy, glaucoma, corneal abrasionsMucoid discharge Allergic conjunctivitis, chlamydial infectionWatery discharge Viral conjunctivitis, chemical irritantsPurulent discharge Bacterial conjunctivitis, corneal ulcer, orbital cellulitis

Adapted from American Academy of Ophthalmology. Managing the red eye [slide presentation]. San Francisco: American Academy of Ophthalmology, 1988. Used with permission.

Itching often suggests an allergic or irritative cause, especially if it is accompanied by a mucoid or stringy discharge. Nasal stuffiness, sneezing and a history of asthma or eczema support an allergic etiology. A scratchy sensation or a feeling of a foreign body often accompanies conditions that lead to dry eye, such as xerophthalmia from Sjogren's syndrome or pingueculae and pterygia from excessive sun and wind irritation or actual foreign bodies.

Burning is a common symptom of lid, conjunctival and corneal disorders, and implies ocular pathology. Local lid tenderness or a lump on the lid indicates a stye or chalazion caused by inflammation of the Moll's glands, meibomian glands or the glands of Zeis.

Ocular pain and photophobia are considered clinically significant symptoms because one or both frequently occur with vision-threatening disorders such as iritis, keratopathy, acute glaucoma and corneal abrasions. Infections such as periorbital cellulitis can also be associated with ocular pain, orbital pain, or both.

Sudden diminution or loss of visual acuity should be considered an ocular emergency and, in the context of red eye, may indicate corneal or uveal tract disorders, acute glaucoma or orbital cellulitis.

Red Eye Associated with Lid Pathology

STYE OR HORDEOLUM

A stye or acute external hordeolum is an infection of the glands of Zeis or Moll's glands along the lash line. It usually develops acutely, points and spontaneously drains within one week (Figure 1). Symptoms include swelling of the eyelid and local pain that can be disproportionate to the size of the stye. The stye is often limited to the lid without causing a red eye. Warm compresses and topical antibiotics may encourage pointing; the affected lash can then be pulled to promote drainage. If spontaneous drainage does not occur, an abscess may have formed, requiring incision and drainage.

[Figure 1 ILLUSTRATION OMITTED]

CHALAZION

A chalazion is a granulomatous reaction in the meibomian gland, a modified sweat gland in the tarsal plate of the lid (Figure 2). It is usually chronic, requiring treatment with incision and drainage, or excision. The chalazion can be secondarily infected by pyogenic cocci and may result in an acute chalazion (acute internal hordeolum). Treatment includes topical application of antibiotics (eye drops during the day and eye ointment at bedtime) and use of warm compresses.

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BLEPHARITIS

Blepharitis is an eyelid inflammation caused by a seborrheic process or bacteria and can be associated with red eye. Seborrheic blepharitis may be a component of seborrheic dermatitis elsewhere on the body. Staphylococcal blepharitis is a more acute form of blepharitis (Figure 3). Symptoms include a foreign-body sensation, burning and accumulation of matter along the edges of the eyelids. Treatment includes warm compresses and gentle debridement with cotton swabs, using nonirritating baby shampoo diluted with water. Commercially available lid scrubs and topical antibiotics may also be used.

[Figure 3 ILLUSTRATION OMITTED]

Red Eye Associated with Discharge

ORBITAL CELLULITIS

Orbital cellulitis can be a complication of primary ocular infection or paranasal sinusitis (classically ethmoid sinusitis in children), often with purulent discharge (Figure 4). The patient is usually febrile and can appear quite toxic. Orbital cellulitis can be a primary infection, or it can result from trauma with secondary infection. Periorbital erythema and edema are usually evident and can cause the eye to swell shut. Orbital cellulitis can lead to acute cavernous sinus thrombosis or meningitis. Treatment includes surgical consultation and parenteral antibiotic therapy.

[Figure 4 ILLUSTRATION OMITTED]

CONJUNCTIVITIS

Conjunctivitis may be caused by bacterial or viral infection, allergies, chemicals or a tear deficiency. Stringy mucoid discharge suggests allergy, especially if it is accompanied by itching and associated with other atopic manifestations (e.g., allergic rhinitis, asthma, eczema). Purulent discharge suggests a bacterial infection, especially if the conjunctival injection is severe. Clear watery discharge can be associated with a viral infection, particularly if preauricular adenopathy is present, but it can also result from chemical irritants.

Allergic conjunctivitis (Figure 5) is frequently associated with other atopic conditions such as hay fever, asthma and eczema. It may follow exposure to various allergens and occur in seasons when pollen counts are high. In addition to red eye, symptoms include stringy mucoid discharge, itching and tearing.[2] This benign disorder is usually seen in late childhood and early adulthood, and it may be seasonal or perennial. Conjunctival edema or chemosis (Figure 6) may be marked and sudden in onset. Vernal and atopic keratoconjunctivitis are other allergic eye diseases that may present as a red eye.[3]

[Figure 5 & 6 ILLUSTRATION OMITTED]

Topical lodoxamide (Alomide), a mast cell stabilizer, is the recommended treatment for mild to moderate allergic eye disease.[4] Levocabastine (Livostin) is the only topical agent that is solely a histamine [H.sub.1] antagonist and has compared favorably with oral antihistamine agents[5] and cromolyn.[6] Ketorolac (Acular) is a nonsteroidal anti-inflammatory drug that has been shown to be useful for the treatment of ocular symptoms related to seasonal allergic conjunctivitis.[7]

Topical vasoconstrictor antihistamines such as Vasocon-A (naphazoline hydrochloride plus antazoline phosphate) and Naphcon-A (pheniramine maleate plus naphazoline) are now available over the counter and are especially useful for the treatment of prominent ocular hay fever symptoms. However, these medicines may produce rebound hyperemia. Verrtal and atopic keratoconjunctivitis often require treatment with steroids. These conditions should be managed in consultation with an ophthalmologist because they are potentially vision-threatening and may be complicated by the development of corneal ulceration or secondary infection with herpes simplex virus.

Although bacterial conjunctivitis (Figure 7) may be caused by a large number of organisms, Staphylococcus species, Streptococcus pneumoniae and Hemophilus species are the usual offenders. These infections are capable of producing a copious purulent discharge. All of these infections (except for gonococcal and chlamydial infections) may be treated with topical antibiotics for two to three days. Neomycin preparations should be avoided because of a higher likelihood of hypersensitivity.

[Figure 7 ILLUSTRATION OMITTED]

EPISCLERITIS AND SCLERITIS

Episcleritis and scleritis are chronic disorders characterized by destruction of collagen, cellular infiltration and vasculitic changes in the sclera.[19] Causes include collagen vascular disorders, granulomatous diseases, metabolic disorders and various infectious agents (Table 2).[20] Constant, boring pain, often severe enough to interfere with sleep, is the most common symptom. The red eye may appear deep violet because of dilation of the deep vascular plexus of the episclera and sclera (Figure 15). Treatment with oral corticosteroids or cyclophosphamide (Cytoxan, Neosar) may be necessary. Ophthalmologic consultation is strongly recommended.

[Figure 15 ILLUSTRATION OMITTED]

TABLE 2Causes of Episcleritis/ScleritisCollagen vascular disorders Granulomatous disorders InfectionsAnkylosing spondylitis Tuberculosis ToxoplasmosisRheumatoid arthritis Sarcoidosis Herpes zosterPolyarteritis nodosa Syphilis Herpes simplexWegener's granulomatosis Leprosy PseudomonasSystemic lupus erythematosus Metabolic disorders Pyogenic cocciPsoriatic arthropathy Thyrotoxicosis Aspergillus Gout

Adapted from O'Connor GR. Uveal tract and sclera. In: Vaughan D, Asbury T, Riordan-Eva P, eds. General ophthalmology. 13th ed. Norwalk, Conn.: Appleton & Lange, 1992:150-68. Used with permission.

PRIMARY ANGLE-CLOSURE GLAUCOMA

Primary angle-closure glaucoma results from closure of a preexisting narrow anterior chamber angle sometimes found in farsighted patients, the elderly (because of physiologic enlargement of the lens) and Asians. Symptoms include severe pain and profound vision loss. The blurred vision may be associated with halos around lights. Headache, nausea, vomiting or abdominal pain may confuse the diagnosis. The red eye may be associated with a steamy cornea and a dilated pupil fixed in the mid position (Figure 16). Tonometry reveals elevated intraocular pressure.

[Figure 16 ILLUSTRATION OMITTED]

Possible precipitants to primary angle closure glaucoma include sitting in a darkened movie theater (which dilates the pupil), stress (causing increased circulating catecholamines) or use of sympathomimetic or anticholinergic medication. Early identification is necessary for prompt ophthalmologic referral. Treatment is urgent and includes lowering of intraocular pressure with the carbonic anhydrase inhibitor acetazolamide (Diamox), 500 mg intravenously or intramuscularly, then 250 mg orally four times daily. Definitive therapy includes laser iridotomy or peripheral iridectomy.[21]

The author thanks the medical editing department of the Kaiser Foundation Research Institute, Oakland, Calif., for providing editorial assistance.

Figures 1 through 5 and 7 through 16 from American Academy of Ophthalmology. Managing the red eye [slide presentation]. San Francisco: American Academy of Ophthalmology, 1988. Used with permission. Figure 6 from Berson FG. Ophthalmology study guide for students and practitioners of medicine. San Francisco: American Academy of Ophthalmology, 1988. Used with permission.

REFERENCES

[1.] American Academy of Ophthalmology. Managing the red eye [slide presentation]. San Francisco: American Academy of Ophthalmology, 1988.

[2.] Friedlaender MH. Immunologic aspects of diseases of the eye. JAMA 1992;268:2869-73.

[3.] Foster CS, Calonge M. Atopic keratoconjunctivitis. Ophthalmology 1990;97:992-1000.

[4.] Caldwell DR, Verin P, Hartwich-Young R, Meyer SM, Drake MM; Efficacy and safety of lodoxamide 0.1% vs cromolyn sodium 4% in patients with vernal keratoconjunctivitis. Am J Ophthalmol 1992; 113:632-7

[5.] Titi MJ. A critical look at ocular allergy drugs. Am Fam Physician 1996;53:2637-42, 2645-6.

[6.] Abelson MB, George MA, Smith LM. Evaluation of 0.05% levocabastine versus 4% sodium cromolyn in the allergen challenge model. Ophthalmology 1995;102:310-6.

[7.] Tinkelman DG, Rupp G, Kaufman H, Pugely J, Schultz N. Double-masked, paired-comparison clinical study of ketorolac tromethamine 0.5% ophthalmic solution compared with placebo eyedrops in the treatment of seasonal allergic conjunctivitis. Surv Ophthalmol 1993;38(Suppl):133-40.

[8.] Riordan-Eva P, Vaughan DG. Eye. In: Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current medical diagnosis & treatment. 35th ed. Stamford, Conn.: Appleton & Lange, 1996:156-80.

[9.] Darougar S, Monnickendam MA, Woodland RM. Management and prevention of ocular viral and chlamydial infections. Crit Rev Microbiol 1989; 16:369-418.

[10.] Lemp MA. Recent developments in dry eye management. Ophthalmology 1987;94:1299-304.

[11.] Rubinfeld RS, Pfister RR, Stein RM, Foster CS, Martin NF, Stoleru S, et al. Serious complications of topical mitomycin-C after pterygium surgery. Ophthalmology 1992;99:1647-54.

[12.] Dart JK. Diseases and risks associated with contact lenses. Br J Ophthalmol 1993;77:49-53.

[13.] Matthews TD, Frazer DG, Minassian DC, Radford CF, Dart JK. Risks of keratitis and patterns of use with disposable contact lenses. Arch Ophthalmol 1992;110:1559-62.

[14.] Torok PG, Mader TH. Corneal abrasions: diagnosis and management. Am Fam Physician 1996;53:25219,2532.

[15.] Mondino BJ. Inflammatory diseases of the peripheral cornea. Ophthalmology 1988;95:463-72.

[16.] Parks DJ, Abrams DA, Sarfarazi FA, Katz HR. Comparison of topical ciprofloxacin to conventional antibiotic therapy in the treatment of ulcerative keratitis. Am J Ophthalmol 1993;115:471-7.

[17.] Berger ST, Mondino BJ, Hoft RH, Donzis PB, Holland GN, Farley MK, et al. Successful medical management of Acanthamoeba keratitis. Am J Ophthalmol 1990;110:395-403.

[18.] Rosenbaum JT. An algorithm for the systemic evaluation of patients with uveitis: guidelines for the consultant. Semin Arthritis Rheum 1990;19:248-57.

[19.] Fong LP, Sainz de la Maza M, Rice BA, Kupferman AK, Foster CS. Immunopathology of scleritis. Ophthalmology 1991;98:472-9.

[20.] O'Connor GR. Uveal tract and sclera. In: Vaughan D, Asbury T, Riordan-Eva P, eds. General ophthalmology. 13th ed. Norwalk, Conn.: Appleton & Lange, 1992:150-68.

[21.] Rosenberg LF. Glaucoma: early detection and therapy for prevention of vision loss. Am Fam Physician 1995;52:2289-98, 2303-4.

JIMMY H. HARA, M.D. is residency program director and assistant chief of service in the Department of Family Practice at the Kaiser Permanente Medical Center in Los Angeles. He is associate clinical professor of family medicine and serves on the executive committee for the University of California, Los Angeles, Multicampus Family Medicine Division. He also acts as regional director of graduate medical education for the Southern California Permanente Medical Group. He received a medical degree from the University of California School of Medicine, San Francisco.

Address correspondence to Jimmy H. Hara, M.D., Department of Family Practice, Kaiser Permanente Medical Center, 4747 Sunset Blvd., Los Angeles, CA 90027-6021.

Each year member of a different family practice department develop articles for "Problem-Oriented Diagnosis." This is the ninth in a series from the Kaiser Permanente affiliated Family Medicine Residency Program of Southern California. Guest editor of the series is Robert Sallis, M.D., from the Kaiser Permanente Medical Center, Fontana, Calif.

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