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How to diagnose the acute red eye with confidence

You can identify and treat many types of conjunctivitis, but you should always know when referral is needed to preserve the patient’s vision and, in some instances, the patient’s life.

CPT Michael Roscoe MS, MPAS, PA-C; CPT Timothy Landis, OD

Mike Roscoe is on the faculty at the Butler University/Clarian Health Physician Assistant Program in Indianapolis, Ind. He also works in the emergency department of Community Hospital of Anderson in Anderson, Ind. Tim Landis is in a private practice in Elizabethtown, Ky. This article was written while they were deployed in Afghanistan with Task Force Phoenix for Operation Enduring Freedom. The authors have indicated no relationships to disclose relating to the content of this article.

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CME

Earn Category I CME credit by reading this article and "Understanding diastolic dysfunction" and successfully completing the post-test. Successful completion is defined as a cumulative score of at least 70% correct.

This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of March 2006.


For an explanation of competencies, click here.

The acute red eye is the most common ocular disorder that primary care medical providers will encounter.1 Most cases of red eye are benign, but sometimes the cause is serious and can lead to permanent vision loss. With limited equipment and resources, the provider can properly diagnose and treat most cases of acute red eye. A red eye tool kit includes a penlight, sodium fluorescein strips, Wood’s lamp or cobalt blue flashlight, and tetracaine. A strong patient history is also essential.

A few simple determinants can be used to ascertain whether the patient presenting with an acute red eye needs immediate referral or can be managed on an outpatient basis. Expensive diagnostic equipment, such as a slit lamp, is not necessary to make the initial diagnosis but should be used to confirm it.

History and physical examination

The history should address nine essential areas: the presence or absence of pain, sensation of foreign body, itching, discharge (and characteristics), light sensitivity, onset, whether vision is affected, recent illnesses/ trauma, and ophthalmologic history (contact lens use, eye surgery, prior history).2

The examination should always cover visual acuity, pupil shape, reactivity, comparison between the pupils, extraocular muscle function, confrontation fields, and palpation for preauricular nodes (PAN).2 Secondary assessments that are helpful, if available, include staining and evaluating the affected eye with sodium fluorescein and a cobalt blue light; measures of intraocular pressures (IOP), and a slit-lamp evaluation.

The most common causes of red eye are viral, allergic, or bacterial conjunctivitis, scleritis, episcleritis, anterior uveitis, angle-closure glaucoma, keratitis, and subconjunctival hemorrhage. This is not a complete list, but with an organized history and good physical examination the clinician will avoid a misdiagnosis, which can add to the potential complications. Table 1 summarizes the findings in patients with acute red eye. Figure 1 provides the basic anatomy of the eye.

Viral conjunctivitis

Conjunctivitis is a general term that refers to any inflammatory condition of the membrane that lines the eyelids and covers the exposed surface of the sclera.3 The most common ophthalmic condition seen by primary care providers,4-6 conjunctivitis is responsible for approximately 30% of all eye complaints.7 Every patient with conjunctivitis should have fluorescein staining in each eye to ensure that a corneal abrasion, ulcer, or herpetic dendrite is not missed.6 The white eye should always be stained first to avoid any cross contamination.

Because it is the leading cause of the acute red eye, viral conjunctivitis should be most prominent in the differential diagnosis (see Figure 2) .1,6 With sudden onset and rapid progression, it is marked by a clear, watery discharge and a global injection pattern.7 There may be a foreign-body sensation with mild pruritus. In severe cases, PAN will be noted on the same side as the ocular infection.7 Although viral conjunctivitis tends to manifest bilaterally, it usually starts in one eye with the other becoming injected a few days later.

Adenoviral infection is the most common cause of viral conjunctivitis and may be sporadic or epidemic.8 No definitive treatment is available for conjunctivitis caused by adenovirus. Supportive care, which is appropriate for minor cases, may include artificial tears for lubrication, cold compresses, topical decongestants, and topical corticosteroids if ocular edema is significant. Replicating virus can be found in 95% of patients 10 days after the appearance of symptoms but in only 5% of patients by day 16.9 Patients should be informed that viral conjunctivitis is highly contagious. Good hand-washing practice is essential for the next 2 weeks, and items that could be contaminated by both direct and indirect means should not be shared.

Herpes simplex virus (HSV) infection, which manifests as light sensitivity and a foreign-body sensation, is the most critical viral infection to identify in the eye. Definitive for diagnosis is the common appearance of a dendritic lesion on the cornea, which you can see easily with sodium fluorescein staining of the cornea and a Wood’s lamp. The corneal lesions of HSV infection may also be confluent and geographic, or even atypical.

A topical or oral antiviral medication such as trifluridine or acyclovir can be used as a first-line treatment for 10 to 14 days.6 Trifluridine is toxic to the cornea, so start with a high dosage and then reduce it quickly. Topical antibiotics can also be used to prevent secondary infection. If a patient with suspected HSV infection has corneal staining, ophthalmic referral is necessary. Corticosteroid use should be avoided because it may increase the risk of secondary bacterial infection.

Herpes zoster (HZ), often referred to as shingles, can also affect the eye. When the ophthalmic branch of the trigeminal nerve is involved, a vesicular lesion may appear at the tip of the nose (Hutchinson’s sign), but this is not pathognomonic for HZ infection. The cornea may reveal a global lesion rather than the dendritic lesion seen with HSV infections; however, the skin lesions distinguish infection with HSV from ocular HZ. Of note, corneal pathology is not always necessary to make the diagnosis of HZ. Approximately 50% of patients with ocular HZ will develop ocular complications; uveitis occurs in approximately 43% of cases.10 One study found that 56% of patients with a diagnosis of ocular HZ developed secondary glaucoma, with 26% needing surgery to control IOP.10

Ocular HZ should be treated with an oral antiviral medication such as acyclovir for 7 to 10 days. There is no evidence that topical agents for HZ infections are effective in the eye.6 Because of the chance of secondary complications, patients with any ocular herpetic infection should see an optometrist or ophthalmologist.

 

Allergic conjunctivitis

The hallmark symptom of allergic conjunctivitis is itching, which is often profound.7 The patient may have other indicators of an allergic reaction, such as watery eyes and nasal congestion. The most common forms of ocular allergy are seasonal allergic conjunctivitis (IgE-mediated hypersensitivity) and sensitivity to allergens such as animal dander or dust.11 The injection pattern for allergy is global, bilateral, and equal between the two eyes. Eye discharge can be clear/watery or mucoid.

The clinician may find it difficult to distinguish between allergic conjunctivitis and viral conjunctivitis based on findings from the physical examination. The key is in the history: Unless the patient reports itching, the condition is not due to allergy.

Treatment for allergic conjunctivitis is similar to treatment for an allergic response anywhere else. This can range from supportive care, such as a cold compresses, to ocular NSAIDs to reduce pain and swelling. Hallmark treatments revolve around histamine-blocking eye drops such as olopatadine (Patanol), pemirolast (Alamast), or ketotifen (Zaditor).

 

Bacterial conjunctivitis

Most bacterial conjunctivitis is due to gram-positive organisms. The three most common pathogens are Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus.1,8 The condition usually comes on abruptly as tearing and ocular irritation in one eye that generally spreads to the opposite eye within 48 hours.12 Mucopurulent discharge typically collects within the eyelashes and causes matting of the eyelids and lashes. Bacterial conjunctivitis manifests as a red eye that has an injection pattern more pronounced at the two fornices.7

Treatment of bacterial conjunctivitis involves several steps, beginning with supportive care. Lubrication will help to move bacteria off the eye and warm compresses will aid the immune response, but the patient often does not follow these recommendations. Definitive treatment includes a topical ophthalmic broad-spectrum antibiotic administered as either ointment or drops. Ointments do not need to be applied as frequently as drops, and they tend to result in some decrease of ocular irritation due to their lubricating nature. However, it is often difficult to place ointments and they will blur vision. Ophthalmic drops are easier to instill but they must be administered more frequently than ointment. They also do not help alleviate acute discomfort. The choice of agent should be based on the patient’s ability to adhere to the prescribed regimen. Adult patients tend to do better with drops than ointments.

Hyperacute conjunctivitis is caused by gonococcal infection in sexually active persons. Although bacterial conjunctivitis generally does not have any long-term effect on vision, hyperacute conjunctivitis can have disastrous effects on a patient’s vision. It is characterized by an abrupt onset of a copious discharge that rapidly worsens and will re-form virtually immediately after wiping the eye. PAN is usually present, with severe swelling of the eyelids.7 There is pain on palpation (close the eyes and lightly push on the globe, through the lid). A patient with this infection requires immediate referral and treatment by an optometrist or ophthalmologist the same day, as hyperacute conjunctivitis will lead to peripheral ulceration and, ultimately, perforation.13 Treatment is with topical and systemic antibiotics. The topical choices are the same as for standard bacterial conjunctivitis, while systemic therapy is also geared toward treating the gonorrhea. It is important to ask about sexual contacts and other signs and symptoms, as this is a highly contagious infection.

 

Episcleritis

The episclera lies beneath the conjunctiva and over the sclera. Episcleritis is a red eye condition that has a rapid onset with sectorial redness involving the episcleral vessels (see Figure 3).8 Generally, neither pain nor discharge is associated with this condition, but there may be some focal tenderness on palpation. Episcleritis is a self-limiting but recurrent condition, with episodes occurring repeatedly over months.1,8 Close examination reveals noninflamed conjunctival vessels, which lie on top of the episcleral vessels. This finding effectively rules out conjunctivitis. Another simple test, if available, is to instill 1 drop of phenylephrine 2.5% into the red eye. The conjunctival vessels will blanch, while the episcleral vessels will remain unaffected. Careful observation with pupil testing limits the possibility of a uveitis reaction.

Treatment options include the use of oral or topical NSAIDs and/or topical corticosteroids (be sure there is no staining on the cornea before prescribing corticosteroids). Reassure the patient of the self-limiting nature of the illness.

 

Scleritis

Scleritis is painful and may be severe. Significant ocular tenderness, tearing, and photophobia may occur.8 On examination the eye may have a bluish red appearance. Associated scleral necrosis and peripheral ulcerative keratitis can impair vision.8 Scleritis is linked to life-threatening vascular or connective tissue disease, most commonly rheumatoid arthritis, in an estimated 30% to 60% of all cases.8,14 In 15% of patients, scleritis is the presenting manifestation of a collagen vascular disorder and may precede additional symptoms by several months. The 8-year mortality rate with this diagnosis is 30%, with death usually due to a vascular disease.15

Palpation of the eye will produce significant, deep ocular pain and tenderness. There may be photophobia but no discharge other than tearing in response to bright light, which is a diagnostic point. The redness pattern does not involve the conjunctival vessels. Topical and oral corticosteroids or NSAIDs help in the interim period. Note that the key to treating patients with scleritis is rapid referral to an optometrist or ophthalmologist along with evaluation for systemic disease.

 

Acute anterior uveitis

Sometimes referred to as iridocyclitis, acute anterior uveitis is an intraocular inflammation involving the anterior ocular structures.8 Its onset is sudden, with ocular pain, photophobia, conjunctival injection, and sometimes blurred vision.8 Acute anterior uveitis will manifest as a paralimbal injection pattern of redness around the iris that is often referred to as iritis. The photophobia, from the inflammatory response in the anterior chamber of the red eye, is manifested as pain and/or a photophobic response to direct and consensual illumination. Additional pupil testing in the red eye will show a constricted, miotic pupil that will react to direct illumination in a sluggish manner. The eye is also tender to touch.

Classic findings include inflammatory cells and proteinaceous flare in the anterior chamber of one eye.1 Note that anterior uveitis and inflammatory cells can trigger acute glaucoma or vision loss. If IOP cannot be measured and immediate referral is not available, refer to an eye care professional as soon as possible. Treatment includes topical corticosteroids; prednisolone acetate 1% is excellent at penetrating the cornea to deliver medication to the anterior chamber. The standard regimen is high dosage and high frequency for the first few days, followed by tapering. A typical schedule might be 1 drop hourly on day one, 1 drop every 2 hours on day two, and then 1 drop 4 times daily for five days. If the corticosteroid is used for less than 10 days, a tapered dosage may not be necessary, but it is the safest way to prevent rebound uveitis.

Acute angle-closure glaucoma

Resulting from the peripheral iris blocking the outflow of fluid from the eye, acute glaucoma manifests as severe ocular pain, redness, and mid-dilated pupil with decreased vision.8 The patient will also complain of blurred vision, halos around lights secondary to corneal edema, and often an associated headache with nausea and vomiting. The episodes or attacks often occur in the evening when reduced ambient illumination provokes mydriasis, causing the accordionlike folds of the peripheral iris to block the outflow of aqueous humor.1 Unless treated quickly, acute glaucoma can cause severe visual loss from damage to the optic nerve.8 Angle-closure glaucoma attacks manifest as a global injection pattern in one eye. Tearing tends to be the only type of discharge, and the cornea often appears steamy or hazy from the increased IOP and corneal edema.

Tonometry greatly enhances the diagnosis, which can be made by looking at the entire constellation of physical findings. A normal IOP reading is 10 to 23 mm Hg.16 A pressure reading greater than 40 mm Hg, combined with the above symptoms, gives the diagnosis of angle-closure glaucoma.16 If a tonometer is not available, a penlight can be used to test the pupil. Acute-angle closure will manifest as a pupil that is mid-dilated (4-6 mm) and nonreactive to direct illumination. Simply put, if the pupil is still moving, it is not an acute-angle closure attack. The loss of pupil movement is a result of the high pressure to prevent normal iris function.

Ideally, prompt and rapid transfer of care to an optometrist or ophthalmologist will be possible. If transfer is delayed for some reason, there are treatments that can prevent vision loss. A simple acute-angle-closure kit (1 bottle of timolol 0.5% and acetazolamide 250 mg tablets, at a total cost of less than $10) will save vision. Once the diagnosis of acute-angle glaucoma is made, instill 1 drop of timolol, followed by another drop 5 minutes later. Have the patient swallow two 250-mg tablets of acetazolamide. Note that this emergency treatment does not replace immediate consultation or transfer to an optometrist or ophthalmologist. Other possible treatments, often the last resort, are the use of hyperosmotic IV or oral preparations to decrease the fluid level inside the eye.

Clinicians should remember that the presenting symptoms of acute angle-closure glaucoma and of migraine headache are very similar but that the morbidity is quite different. All eye examinations, with pupil reactivity, should be documented in patients with migraine headaches.

 

Keratitis

When exploring a diagnosis of keratitis, the clinician should stain the eye to look for uptake on the cornea. If the patient has positive findings on the cornea or a history of a possible foreign body that entered the eye at high speed, the problem should be considered an ocular emergency and immediate ophthalmologic consultation should be obtained (see Figure 4).

Superficial keratitis (dry eye syndrome [DES]) should be at the top of the differential diagnosis in geriatric patients. This condition is characterized by inflammation of the corneal epithelium and superficial stroma.1 The typical injection pattern is global and bilateral. The diagnosis is difficult without fluorescein staining and a slit-lamp examination. One diagnostic method is to ask the patient not to blink for as long as possible; if blinking occurs in less than 10 seconds or if the stain breaks up and turns black in less than 10 seconds, the patient has DES. Multiple punctate lesions and erosions are visible with a slit lamp. Often only gray spots can be seen, imparting a hazy appearance to the cornea.1

Patients who have superficial keratitis are at higher risk for other forms of infection. This can best be remembered as “a warm, wet eye stays healthy, and a cold, dry eye gets sick.”

Treatment for superficial keratitis is lubrication. Patients will tend to use artificial tears 2 to 10 times daily. Ointment can also be used at bedtime. If the keratitis is severe enough, the patient should see an ophthalmologist or optometrist for punctal occlusion treatment.

Bacterial keratitis, commonly known as corneal ulcer, is primarily caused by staphylococci and streptococci, although people who wear contact lenses tend to get pseudomonal infections as well.6 Patients will present with rapidly progressing pain, ocular redness, photophobia, and a purulent discharge. The cornea will often appear hazy on simple visual inspection. Fluorescein staining can easily demonstrate the ulcer, the presence of which differentiates bacterial keratitis from conjunctivitis. A lesion that is white on visual inspection and stains with fluorescein is an ulcer.

Treatment consists of topical fluoroquinolones (eg, ciprofloxacin) because of the high rate of gram-negative bacteria. Many optometrists and ophthalmologists will add an oral fluoroquinolone to the regimen. Lubricating drops and ointments may also help to relieve some of the associated discomfort. The patient with bacterial keratitis should be followed closely, and ophthalmic referral should be obtained.

Subconjunctival hemorrhage

The diagnosis of subconjunctival hemorrhage, a painless red eye without discharge, is based on simple observation. The injection pattern is unique because it has clear borders and masks the conjunctival vessels. When viewed through the almost transparent conjunctiva, a subconjunctival hemorrhage appears as fresh red blood against a white scleral background. The condition can manifest spontaneously and will alarm the patient as well as the inexperienced clinician. In most cases vision is not affected, and the patient may report a history of trauma, often very slight. Subconjunctival hemorrhage can also occur with Valsalva maneuvers, such as from protracted vomiting or coughing, or with a history of anticoagulant use. Consider staining the eye with fluorescein to rule out trauma to the cornea if a patient presents with any type of pain in the eye.

Treatment consists of explaining possible causes of the hemorrhage and reassuring the patient that there is no immediate danger to vision. A high-profile subconjunctival hemorrhage will take about 10 to 14 days to resolve. The second aspect of treatment is evaluating contributory factors. Consider recommending a warm compress and lubrication. Both may be marginally helpful in reducing the recovery period by 1 to 3 days.

 

Conclusion

The acute red eye has many possible causes and presents a challenge to the generalist clinician. Many cases are benign, but others can have devastating consequences if not quickly and properly diagnosed. A few simple questions and tests can lead to diagnosis in most cases of acute red eye.   

REFERENCES

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David SP. Should we prescribe antibiotics for acute conjunctivitis? Am Fam Physician. 2002;66(9):1649-1650.  
 

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Kane KY, Meadows S, Ellis MR. Clinical inquiries. When should acute nonvenereal conjunctivitis be treated with topical antibiotics? J Fam Pract. 2002;51(4):312.  
 

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Manners T. Managing eye conditions in general practice. BMJ. 1997;315:816-817.  
 

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Jackson WB. Acute red eye: diagnosis and treatment guidelines. University of Ottawa Eye Institute. 2004. Available at: http://www.eyeinstitute.net/redeye.pdf. Accessed January 20, 2006.  
 

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Elnifro EM, Cooper RJ, Klapper PE, et al. Diagnosis of viral and chlamydial keratoconjunctivitis: which laboratory test? Br J Ophthalmol. 1999;83:622-627.  
 

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Thean JH, Hall AJ, Stawell RJ. Uveitis in herpes zoster ophthalmicus. Clin Experiment Ophthalmol. 2001;29(6):406-410.  
 

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Friedlaender MH. Conjunctivitis of allergic origin: clinical presentation and differential diagnosis. Surv Ophthalmol. 1993;38(suppl):105-114.  
 

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Leibowitz HM. Antibacterial effectiveness of ciprofloxacin 0.3% ophthalmic solution in the treatment of bacterial conjunctivitis. Am J Ophthalmol. 1991;112(4 suppl):29S-33S.  
 

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Soukasian SH, Baum J. Bacterial conjunctivitis. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea. St Louis, Mo: Mosby; 1997:759-766.  
 

14.

Foster CS, Forstot SL, Wilson LA. Mortality rate in rheumatoid arthritis patients developing necrotizing scleritis or peripheral ulcerative keratitis. Effects of systemic immunosuppression. Ophthalmology. 1984;91(10):1253-1263.  
 

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McGill University Medical School. Red eye; nontraumatic red eye. 2004. Available at: http://www.medicine.mcgill.ca/ophthalmology/Academic/Med%20students/Lectures/RED%20EYE.pdf. Accessed January 20, 2006.  
 

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Bertolini J. Glaucoma, acute angle-closure. eMedicine. Available at: http://www.emedicine. com/emerg/topic752.htm. Accessed January 20, 2006.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 







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