Patching has not been found to improve healing or comfort;13 instead, it delays healing.14,15 The “pirate patch,” which hovers over the eye, does not keep the eyelid down and therefore is not recommended.9
Follow up within 24 hours of initiating treatment to assure that the abrasion is healing. If it appears to be getting worse or is simply not improving, an immediate referral to an ophthalmologist is needed. Abrasions caused by contact with potentially infected material (eg, farm equipment, tree branches, or soil) require daily monitoring until they heal.11
This patient has optic neuritis, caused by inflammation of the optic nerve and disruption of the nerve’s myelin sheath. It predominantly affects young adults, and is more common in women than in men.16 The incidence of optic neuritis is higher among Asians, black South Africans, and children under the age of 15.17,18
Optic neuritis is characterized by monocular (90%) or binocular (10%) complete or partial vision loss, photopsia (flashes of light), and eye pain. Up to 60% of pediatric patients present with blurred vision, bilateral involvement,19 and no pain, while adults predominantly have pain and unilateral vision loss.20 Optic neuritis is often a presenting symptom of multiple sclerosis (MS).16
Physical exam findings in optic neuritis include a sluggish direct light reflex, loss of visual acuity and color vision, as well as acute eye pain.18 Ophthalmoscopic exam may reveal papillitis with edema of the optic disc.21 In the Optic Neuritis Treatment Trial (ONTT), however, only one-third of patients presented with papillitis and swelling of the optic disc.22
MRI of the brain with gadolinium contrast is generally used to confirm the diagnosis. On MRI, 95% of patients with optic neuritis have signs of inflammation of the optic nerve and/or white matter changes consistent with MS (periventricular and ovoid demyelination).23,24
Patients with evidence of demyelination should also be evaluated for MS and other demyelinating disorders. In the ONTT trial, the risk of developing MS within 15 years of an optic neuritis diagnosis was as low as 25% (95% confidence interval [CI], 18%-32%) for patients with no lesions on a baseline brain MRI and as high as 72% (95% CI, 63%-81%) for those with one or more lesions on a baseline MRI, according to the study’s final follow-up.22
The recommended treatment for optic neuritis is intravenous (IV) methylprednisolone 250 mg every 6 hours for 3 to 5 days, followed by oral prednisone at 1 mg/kg/d for 7 to 10 days. Vision usually returns slowly over the course of several months to a year. Ophthalmology consultation should be considered to rule out other causes of optic neuritis.25
Uveitis is often associated with systemic disease or infection, and diagnosis is typically suspected based on a history of conditions such as sarcoidosis, juvenile idiopathic arthritis, Kawasaki’s disease, Sjögren’s syndrome, toxoplasmosis, human immunodeficiency virus (HIV), tuberculosis (TB), syphilis, herpes simplex, and herpes zoster.26
Signs and symptoms vary depending on the part of the uveal tract that’s involved. Anterior uveitis, or iritis, is associated with pain, photophobia, redness, and a varying degree of vision loss. Posterior and intermediate uveitis are less likely to be associated with pain, but can be accompanied by decreased visual acuity and floaters.27
Visual acuity in patients with uveitis can range from normal to varying degrees of vision loss. Redness around the iris can be seen; conjunctival infection is most marked around the circumference of the corneal limbus rather than more peripherally, as seen in conjunctivitis. On slit lamp examination, the beam of light can be seen in the aqueous humor due to protein and leukocyte accumulation—a phenomenon known as “flare.” The pupillary light reflex may be abnormal, and the pupillary opening may be irregular rather than round due to anterior and posterior synechia.28
Patients should be referred to an ophthalmologist for management of the immediate condition and to prevent or treat complications such as vision loss, optic nerve damage, and glaucoma. Acute management includes topical steroids, such as prednisolone acetate ophthalmic 1% 2 to 4 times daily, as well as treatment of the underlying condition. Long-term management varies, depending on the cause of the uveitis.26,29
If the etiology is unknown, a workup should be considered to identify inflammatory and infectious disorders that might be causing uveitis. Chest radiograph is a good beginning to look for evidence of sarcoidosis or TB; serologic testing for syphilis, HIV, and lupus may also be considered.26,29
This patient has viral keratitis caused by herpes. While the pain and foreign body sensation are the same for bacterial and viral keratitis, herpesvirus is distinguishable by the branching opacity that develops on the cornea.
Varicella zoster is the most common cause of viral keratitis, although it can also be caused by herpes simplex and adeno-virus. Because a person who is infected with herpes has the virus for life, however, multiple attacks are possible. Reactivation is associated with stress and a weakened immune system, but may occur spontaneously, as well. Patients who wear contact lenses are no more likely than those who don’t to be infected with the herpesvirus.
Bacterial keratitis is often associated with contact lenses, particularly when they’re continually worn, but also with normal wear.30 Immunosuppression, dry ocular surfaces, and topical corticosteroid use may predispose patients to bacterial keratitis, as well.12Staphylococcus aureus, Pseudomonas aeruginosa, coagulase-negative Staphylococcus, diphtheroids, and Streptococcus pneumoniae are the most common pathogens.31
Patients with keratitis typically complain of eye pain, a sensation of having a foreign body in the eye, photophobia, tearing, and vision changes; a mucopurulent discharge is sometimes present, as well.3 The condition is easily distinguished from conjunctivitis, which typically does not involve eye pain or vision changes.
Visual acuity may be affected if the lesion or corneal edema involves the visual axis. Physical exam in a patient with bacterial keratitis sometimes shows a gray or white corneal opacity, along with corneal erythema. As already noted, a penlight exam will reveal a branching opacity in patients with herpes keratitis.30
Patients with keratitis should be referred immediately to an ophthalmologist32 for a slit lamp evaluation, treatment, and close follow-up.
Corneal cultures can be difficult to obtain, but before prescribing antibiotics, an attempt to collect samples should be made. This can be done—after the administration of topical anesthesia—with a sterile calcium alginate swab. Gently swab the cornea and then inoculate the appropriate gels or mediums. Avoid contact with lashes and eyelids to prevent culture contamination.32
When herpesvirus is suspected, start the patient on an antiviral agent such as trifluridine ophthalmic (1%) 9 times a day, vidarabine ophthalmic (3%) 5 times daily, or 400 mg oral acyclovir 5 times a day. Patients with bacterial keratitis should be started on antibiotic eye drops with Pseudomonas coverage, such as ofloxacin (0.3%), ciprofloxacin (0.3%), or tobramycin (0.3%), 6 to 8 times a day.9
- Foster PJ, Johnson GJ. Glaucoma in China: how big is the problem? Br J Ophthalmol. 2001;85:1277–1282.
- American Academy of Ophthalmology. Preferred Practice Pattern Guidelines. Primary angle closure PPP - October 2010. Available at: http://one.aao.org/CE/PracticeGuidelines/PPP_Content.aspx?cid=92bea8f6-5459-49a6-9233-4528343dc4c3. Accessed July 12, 2012.
- Sau SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology. 2003;110:1878–1879, 1930.
- Leibowitz HM. The red eye. N Engl J Med. 2000;343:345–351.
- Shields SR. Managing eye disease in primary care. Part 3. When to refer for ophthalmologic care. Postgrad Med. 2000;108:99–106.
- Awasthi P. Srivastava SN. Role of oral glycerol in glaucoma. Br J Ophthalmol. 1965;49:660–666.
- Quigley HA. Glaucoma. Lancet. 2011;377:1367–1377.
- Peyman GA, Rahimy MH, Fenandes ML. Effects of morphine on corneal sensitivity and epithelial wound healing: implications for topical ophthalmic analgesia. Br J Ophthalmol. 1994;78:138–141.
- Schein OD. Contact lens abrasions and the nonophthalmologist. Am J Emerg Med. 1993;11:606–608.
- Goldschmidt P. Effects of topical anaesthetics and fluorescein on the real-time PCR used for the diagnosis of herpesviruses and acanthamoeba keratitis. Br J Ophthalmol. 2006;90:1354–1356.
- Benson WH, Snyder IS, Granus V, et al. Tetanus prophylaxis following ocular injuries. J Emerg Med. 1993;11:677–683.
- DeBroff BM, Donahue SP, Caputo BJ, et al. Clinical characteristics of corneal foreign bodies and their associated culture results. CLAO J. 1994;20:128–130.
- Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database Syst Rev. 2006;(2):CD004764.
- Kaiser PK. A comparison of pressure patching versus no patching for corneal abrasions due to trauma or foreign body removal. Corneal Abrasion Patching Study Group. Ophthalmology. 1995;102:1936–1942.
- Clemons CS, Cohen EJ, Arentset JJ, et al. Pseudomonas ulcers following patching of corneal abrasions associated with contact lens wear. CLAO J. 1987;13:161–164.
- Balcer LJ. Clinical practice. Optic neuritis. N Engl J Med. 2006;354:1273–1280.
- De la Cruz J, Kupersmith MJ. Clinical profile of simultaneous bilateral optic neuritis in adults. Br J Ophthalmol. 2006;90:551–554.
- Hwang JM, Lee YJ, Kim MK. Optic neuritis in Asian children. J Ped Ophthalmol Strabismus. 2002;39:26–32.
- Lana-Peixoto MA, Andreade GC. The clinical profile of childhood optic neuritis. Arq Neuropsiquiatr. 2001;59(2-B):311–317.
- Boomer JA, Siatkowski RM. Optic neuritis is adults and children. Semin Ophthalmol. 2003;18:174–180.
- Lucchinetti CF, Kiers L, O’Duffy A, et al. Risk factors for developing multiple sclerosis after childhood optic neuritis. Neurology. 1997;49:1413–1418.
- Optic Neuritis Study Group. Multiple sclerosis risk after optic neuritis: final optic neuritis treatment trial follow-up. Arch Neurol. 2008;65:727–732.
- Wray SH. Optic neuritis. In: Principles and Practice of Ophthalmology. Albert DM, Jakobiec FA, eds. WB Saunders; Philadelphia, Pa: 1994.
- Hickman SJ, Toosy AT, Miszkiel KA, et al. Visual recovery following acute optic neuritis—a clinical, electrophysiological and magnetic resonance imaging study. J Neurol. 2004;251:996–1005.
- Sellebjerg F, Nielsen HS, Frederiksen JL, et al. A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology. 1999;52:1479.
- Rosenbaum JT, Wernick R. The utility of routine screening of patients with uveitis for systemic lupus erythematosus or tuberculosis. A Bayesian analysis. Arch Ophthalmol. 1990;108:1291–1293.
- Jabs DA, Nussenblatt RB, Rosenbaum JT. Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol. 2005;140:509–516.
- Darrel RW, Wagener HP, Kurland LT. Epidemiology of uveitis. Incidence and prevalence in a small urban community. Arch Ophthalmol. 1962;68:502–514.
- Rosenbaum JT, Rahn DW. Prevalence of Lyme disease among patients with uveitis. Am J Ophthalmol. 1991;112:462–463.
- Limberg MB. A review of bacterial keratitis and bacterial conjunctivitis. Am J Ophthalmol. 1991;112(4 suppl):2S–9S.
- Hindman HB, Patel SB, Jun AS. Rationale for adjunctive topical corticosteroids in bacterial keratitis. Arch Ophthalmol. 2009;127:97–102.
- Kaye SB, Rao PG, Smith G, et al. Simplifying collection of corneal specimens in cases of suspected bacterial keratitis. J Clin Microbiol. 2003;41:3192–3197.
CORRESPONDENCE Uyen Michelle Le, MD, 967 Galindo Court, Milpitas, CA 95035; firstname.lastname@example.org
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