Red Eye Case File

Red Eye Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 29

A 60-year-old woman with hypertension and diabetes presents to the emergency department (ED) with severe left eye pain, redness, and blurred vision for 3 hours. She reports that her symptoms began while watching a movie in the local cinema. She initially thought that she had eyestrain, but then her eye began to progressively ache. She denies any symptoms in her right eye. The patient denies preceding trauma, photophobia, ocular discharge, increased tearing, or prior eye surgery. She occasionally wears nonprescription reading glasses because she is farsighted. There are no prior similar events. She also reports seeing colored halos around the light fixtures in the ED, and having a headache over her left brow, some nausea, and one episode of vomiting. She denies dizziness, weakness, imbalance, abdominal pain, or chest pain. She is fully compliant with her medications, She also and reports having taken an over-the-counter cold medicine for nasal congestion for the past 2 days.

On examination, her blood pressure is 155/88 mm Hg, pulse is 88 beats per minute, respirations are 18 breaths per minute, and temperature is 36.8°C (98°F). She is alert, but in obvious discomfort, although able to tolerate ambient light. She has no periorbital signs of trauma. The left conjunctiva has ciliary flush (circumferential reddish ring around the cornea), but no discharge or visible foreign body. Visual acuity is 20/30 in the right eye; but only finger counting in the left eye. Visual fields are grossly intact. Gentle palpation of the closed left eye reveals that it is much firmer than the right. Her left pupil is 5 mm, fixed, and unreactive. Her right eye appears normal; the pupil is 3 mm and briskly reactive. She does not experience pain in the left eye when direct light is applied to the right eye (absent consensual photophobia). Extraocular movements are intact and non-painful. The left cornea is slightly cloudy, which makes fundoscopy difficult. The right fundus appears normal. Her temporal arteries are pulsatile and nontender. The rest of the physical examination, including the remainder of the neurological examination, is normal.

⯈ What is your next diagnostic step?

⯈ What is the most likely diagnosis?

⯈ What is your next therapeutic step?

ANSWER TO CASE: 29

Red Eye

Summary: This is a 60-year-old woman with acute onset of left eye redness, pain, and markedly decreased visual acuity. The left eye feels firmer to palpation than the right eye. The left cornea is edematous with a fixed and dilated pupil.

• Next diagnostic step: Slit-lamp examination should be performed and intraocular pressures must be measured in both eyes. The intraocular pressures, measured using a Tono-Pen are 18 mm Hg and 52 mm Hg in the right and left eye, respectively. Slit-lamp examination reveals bilateral narrow anterior chambers. Cell and flare (inflammatory changes) are absent. There is no evidence of hyphema (blood) or hypopyon (white cells) in the anterior chamber. Fluorescein staining is unremarkable.
• Most likely diagnosis: Acute angle-closure glaucoma.
• Next step: Lowering the intraocular pressure (IOP) should be initiated as quickly as possible to preserve vision.

ANALYSIS

Objectives

1. Become familiar with the vision-threatening causes of a painful red eye.
2. Understand the basic treatment modalities and disposition options for visionthreatening causes of a painful red eye.
3. Recognize the clinical settings, signs, and symptoms, as well as complications, of acute angle-closure glaucoma.
4. Understand the key treatment modalities for angle-closure glaucoma.

Considerations

This 60-year-old woman complains of non-traumatic acute onset of left eye pain, redness, and vision loss with a significant increase in IOP noted on examination. This case is an example of acute angle-closure glaucoma (AACG), a true ophthalmologic emergency characterized by rapidly elevated intraocular pressure, which compromises blood flow to the optic nerve and can result in permanent vision loss. It is likely that her underlying narrow ant chamber angle, plus the combination being in dim lighting and taking an over the counter decongestant (usually a sympathomimetic or anticholinergic), limited outflow of aqueous humor, as the cornea and iris apposed one another.

Approach To:

Red Eye

ACUTE ANGLE-CLOSURE GLAUCOMA

The mechanism of AACG or primary angle-closure glaucoma is pupillary block of the trabecular meshwork outflow pathway. Normally, aqueous humor is produced by the ciliary body in the posterior chamber, and diffuses through the pupil into the anterior chamber where it is drained via the trabecular meshwork. A balance exists between aqueous humor production and outflow to maintain a normal IOP. However, some individuals are predisposed to acute angle closure glaucoma from aqueous humor outflow obstruction secondary to anatomical and environmental factors. Many other forms of glaucoma have a far more insidious, benign presentation, with an inexorable loss of vision. Delay in diagnosis and treatment of AACG results in permanent loss of vision, as the increased IOP causes optic nerve ischemia. The provider must always consider this diagnosis because it is possible to get sidetracked evaluating the associated symptoms of headache, nausea, vomiting or abdominal pain, by looking for neurologic or gastrointestinal etiologies. Risk factors for a narrow angle closure include age-related lens thickening and hyperopia (farsightedness), which results in a shortened eyeball, and a relatively shallow anterior chamber. There is a 75% risk of a similar attack in the fellow eye if left untreated. Medications which cause pupil dilatation can also trigger AACG, including anticholinergics, tricyclic antidepressants, adrenergic agonists, and topical mydriatics.

The incidence of narrow angles in the United States is 2% in white patients, and the rate of AACG is 0.1% in these individuals. Globally, the highest prevalence rates of AACG occur in certain Asian groups, for example, Mongolians and Inuits. African Americans have much higher rates of chronic angle-closure glaucoma (CACG) but lower rates of AACG. Persons between ages of 55 and 65 years have the highest incidence of AACG. The incidence in women is three to four times the rate in men. AACG is likely to occur in 33% to 50% of a patient’s first-degree relatives, so the patient should inform their family members.

Acute angle-closure glaucoma can occur with stress, fatigue, dim lighting, or sustained work at close range. The patient may present with mild unilateral eye ache or intense pain, blurring, nausea, vomiting, abdominal pain, diaphoresis, and frontal headache. The hallmarks of the physical examination include a fixed, dilated, midposition pupil, diffuse conjunctival injection, corneal edema (clouding), and a shallow anterior chamber (Figure 29–1). Slit-lamp examination may reveal mild cell and flare, but no hyphema or hypopyon. The IOP will be elevated (normal is 9-21 mm Hg); pressures can reach 80 mm Hg in AACG. The other eye must always be examined for anterior chamber depth (the angle is usually narrow) and IOP.

Management

The therapeutic goal of the initial management of acute angle-closure glaucoma is to decrease IOP by decreasing aqueous production and increasing outflow. The principal treatment modalities include aqueous suppressants, osmotic agents, and miotic agents.

Figure 29–1. Acute angle-closure glaucoma. Pupil is mid-dilated, fixed, and the cornea is cloudy.

(Reproduced, with permission, from Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine.

6th ed. New York, NY: McGraw-Hill;2004:1460.)

After corneal edema subsides, the definitive treatment is a laser peripheral iridectomy, performed by an ophthalmologist.

Treatment to lower the intraocular pressure should be initiated in the ED in consultation with an ophthalmologist. Intraocular pressure is first lowered by decreasing aqueous humor production with agents such as topical β-blockers (timolol 0.5%), an α-2-agonist (apraclonidine), and a carbonic anhydrase inhibitors (acetazolamide 500 mg orally or IV). Patients with sulfa allergy may not tolerate acetazolamide. Osmotic agents, such as mannitol and glycerol, can be used instead of acetazolamide to dehydrate the vitreous humor, which decreases intraocular fluid volume, and thus lowers IOP. Mannitol may induce hypotension in patients with poor cardiac function, and glycerol should be avoided in diabetic patients. Miotics (pilocarpine) enhance trabecular outflow by constricting the pupil to disrupt the corneal-iris apposition. Intraocular pressure should be first lowered by the administration of topical β-blockers and acetazolamide prior to the administration of pilocarpine as the ischemic iris sphincter may be unresponsive to pilocarpine at extremely high intraocular pressures (>50 mg Hg). Pilocarpine is only used in patients with native lenses since pilocarpine will induce movement in artificial lens. Systemic concerns related to topical β-blocker administration include asthma, severe chronic obstructive pulmonary disease (COPD), bradycardia, heart block, congestive heart failure, and myasthenia gravis. Systemic absorption of topical agents can be reduced up to 70% by instructing the patient to close his or her eyes while occluding the lower tear ducts at the root of the nose after applying the drops. Punctal occlusion decreases drug absorption by the nasal mucosa. The patient should also receive analgesic and antiemetic medications.

Differential Diagnosis of the Red Eye

Other vision-threatening and painful causes of a red eye include severe conjunctivitis, keratitis, corneal ulcer, anterior uveitis, endophthalmitis, orbital cellulitis, scleritis, and temporal arteritis (Table 29–1). Causes of acute vision loss are outlined in Table 29–2.

In this case, the absence of any discharge makes the possibility of conjunctivitis highly unlikely, but discharge can be scant. However, gonococcal conjunctivitis (the most serious form of bacterial conjunctivitis) produces a copious purulent discharge with an intensely red eye, and may potentially perforate the cornea. With chlamydial conjunctivitis the clinical course is more chronic; although the conjunctivae are very red, there is scant discharge. The incidence of sexually transmitted chlamydial conjunctivitis is increasing.

Corneal inflammation, or keratitis, may be due to viral, bacterial, or protozoal infection, contact lenses, trauma, or ultraviolet light. Severe keratitis can progress to a corneal ulcer, which may be visible to the unaided eye as a white defect. Distinguishing an ulcer from a corneal abrasion is clinically significant and can

be challenging. Examination with the slit lamp is required. The major distinction is the hazy/cloudy stroma that lies beneath the ulcer in contrast to the clear stroma deep to most abrasions. A slit-lamp examination is a necessary part of the evaluation of all patients with a red eye. Fluorescein staining should be included in every examination and may be the only way to identify the classic dendrite with terminal bulb markings found in herpes simplex keratitis. Herpes zoster dendrites taper at their ends and are typically associated with periorbital dermatomal vesicular eruptions, or lesions at the tip of the nose (Hutchinson sign of nasociliary involvement). Patients with HIV are at risk for complications of herpes zoster virus (HZV), and must undergo careful corneal and retinal evaluation to prevent vision loss.

Anterior uveitis (iritis) is associated with pain, blurred vision, photophobia (direct and consensual), circumcorneal redness, and anterior chamber cells and flare. A hypopyon (layer of white cells) may be visible along the inferior rim of the anterior chamber. The affected pupil is smaller, irregular, and minimally reactive. IOP can be elevated. Etiologies include idiopathic, infectious (tuberculosis, syphilis, herpes simplex/zoster, toxoplasmosis, cytomegalovirus [CMV]), autoimmune (sarcoidosis, collagen-vascular diseases, human leukocyte antigen [HLA] B27-associated), and post-traumatic. Uveitis due to herpes simplex virus (HSV) and HZV is common in HIV positive patients. Because treatment involves topical corticosteroids with their attendant risk of glaucoma, cataracts, or reactivation of herpes simplex infections, patients should be referred to an ophthalmologist. An immune recovery uveitis occurs in 15.5% of HIV-positive patients with CMV retinitis.

Endophthalmitis is inflammation of the vitreous humor and can be endogenous, secondary to hematogenous spread from a distant site, or exogenous from inoculation after penetrating trauma. Traumatic endophthalmitis usually develops within three days of penetrating injury, retained foreign body, or ocular surgery. Hallmarks include decreased vision, eye pain, hypopyon, anterior chamber cells and flare, anabsent red reflex, and a hazy vitreous. Varying degrees of eyelid swelling, chemosis (conjunctival swelling), and severe conjunctival injection will also be present. Causative organisms include Bacillus cereus, coagulase-negative Staphylococcus, Streptococcus, gram-negative rods, and fungi. Any patient with a hypopyon requires an emergent ophthalmology consult. Orbital CT or ultrasound B-scan microscopy (UBM) may help diagnose a foreign body. Systemic and intravitreal antibiotics will be necessary to preserve any remainder of vision.

Orbital cellulitis, defined as infection deep to the orbital septum, is usually associated with blurred vision, diplopia, conjunctival injection, lid swelling, proptosis, fever, toxicity, and limited or painful ocular motility. An orbital computed tomography (CT) (axial and coronal cuts) is diagnostic, and will often reveal sinusitis (often ethmoid). Admission and parenteral antibiotics are indicated, because of the infection can potentially spread into the brain. Preseptal or periorbital cellulitis is a superficial and far less serious entity but it can be difficult to distinguish from orbital cellulitis. In general, these patients are less toxic appearing, with less pain. Most of these patients can be discharged on oral antibiotics with close follow-up to make sure they didn’t have an early presentation of the more serious orbital cellulitis.

Subconjunctival hemorrhages should be painless and not affect vision. These hemorrhages are often spontaneous or may be associated with minor trauma including coughing and sneezing. In the setting of blunt trauma, continue evaluating for hyphema, globe rupture, or retrobulbar hemorrhage if the patient complains of pain or vision changes. Patients should be informed that the redness (bruise) might take weeks to spontaneously resolve.

Blunt trauma to the eye may result in a hyphema (blood in the anterior chamber) and painful, blurred vision. Blood may be visible to the unaided eye if it layers, or it may only be seen with the slit-lamp in the anterior chamber (microhyphema) on maximum magnification. Initial treatment includes elevating the head 30 degrees, an eye shield to prevent additional trauma, mydriatics to paralyze the ciliary body allowing the iris to rest, pain medication, antiemetics, and consultation. Complications include staining of the cornea by the red cells producing a partially opaque cornea, elevated IOP secondary to red blood cells occluding the trabecular outflow tract, and rebleeding.

Scleritis symptoms include severe eye pain, redness, and decreased vision. An underlying systemic disorder, such as a connective tissue disease, autoimmune disorder, herpes simplex virus (HSV), herpes zoster, HIV, Lyme disease or syphilis, is frequently the cause. Rheumatoid arthritis is the most common systemic cause of scleritis. HZV is the most common infectious cause of scleritis. The conjunctival, episcleral, and scleral vessels are inflamed, either diffusely or focally. Unlike episcleral vessels, which blanch with topical vasoconstrictors and move under cotton swabs, scleral vessels do not. Additionally, the entire sclera may have a bluish or violaceous hue and may be very tender upon palpation. Treatment of the underlying disorder may involve systemic corticosteroids, immunosuppressive therapy, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Temporal arteritis is associated with an ischemic optic neuropathy causes vision loss. These patients often present with temporal artery tenderness, temporal headache, or jaw claudication. Patients are usually older than age 50 years, and will have an elevated erythrocyte sedimentation rate (ESR) and an afferent pupillary defect (contracts to indirect light but not to direct light). A temporal artery biopsy showing giant cells is required for definitive diagnosis. Timely treatment with systemic steroids may prevent blindness in the other eye.

Optic neuritis is caused by demyelinating inflammation of the optic nerve that is highly associated with multiple sclerosis and typically occurs within the third decade of life. These patients complain of subacute eye pain (worse with extraocular movements), vision loss, and decreased color perception (more prominent with red). On examination the eye may appear grossly normal but there will be an afferent pupillary defect (absent papillary response to direct light) and edema of the optic nerve disc on fundoscopy in the affected eye. MRI is useful for confirming optic nerve inflammation and screening for underlying lesions suggestive of multiple sclerosis. Treatment involves hospital admission for intravenous steroids.

Other causes of non-traumatic acute vision loss are listed in Table 29–2 and focus on posterior chamber pathology that present with acute painless vision loss: these including retinal detachment, central retinal artery occlusion, central retinal vein occlusion, vitreous hemorrhage, and posterior vitreous detachment.

COMPREHENSION QUESTIONS

29.1 A 40-year-old man complains of the acute onset of left eye redness with circumcorneal injection (ciliary flush) and pain with bright lights. On examination, his pupil is small and minimally reactive with cell and flare noted on slit lamp examination. He also has pain in the affected eye when light is directed in the unaffected eye (consensual photophobia). Which of the following is the most likely diagnosis?

A. Acute angle-closure glaucoma

B. Anterior uveitis

C. Herpes simplex virus infection

D. Corneal abrasion

29.2 A 50-year-old woman is diagnosed with acute angle-closure glaucoma. She has acutely decreased visual acuity. Which of the following is the most likely mechanism for this condition?

A. Increased IOP caused by increased aqueous humor production

B. Nonreactive pupil leading to increased intraocular pressure

C. Decreased outflow of the aqueous humor

D. Separation of the retina leading to decreased visual acuity

29.3 A 50-year-old woman with redness, severe pain, a bluish scleral tinge, and decreased vision in her right eye is noted to have scleritis. Which of the following is the most common condition associated with scleritis?

A. Systemic lupus erythematosis

B. Rheumatoid arthritis

C. Inflammatory bowel disease

D. Syphilis

29.4 A 36-year-old woman has been diagnosed with glaucoma. She also has asthma which has been well controlled. After using the drops prescribed for her glaucoma, she develops an exacerbation of her asthma. Which of the following medications is most likely responsible for her asthmatic exacerbation?

A. Anticholinergic agent

B. β-blocker agent

C. Alpha-agonist agent

D. Beta-agonist agent

ANSWERS

29.1 B. Anterior uveitis usually presents as photophobia, red eye with pain, and cell

with flare are noted on slit-lamp examination.

29.2 C. In acute angle-closure glaucoma the sudden rise in IOP is a consequence of blocked outflow, usually due to a pupillary block, and not increased production of aqueous humor.

29.3 B. Rheumatoid arthritis is the most common systemic disease associated with scleritis.

29.4 B. Bronchospasm is associated with the use of topical β-blockers which can be systematically absorbed.

CLINICAL PEARLS

⯈ A useful working differential diagnosis for vision-threatening causes of red eye includes acute angle-closure glaucoma, anterior uveitis, endophthalmitis, corneal ulcer, corneal infection, chlamydial/gonococcal conjunctivitis, orbital cellulitis, hyphema, retrobulbar hemorrhage, and scleritis.

⯈ Subconjunctival hemorrhages should be painless and does not affect vision. In the setting of blunt trauma, continue evaluating for hyphema, hypopyon, globe rupture, endophthalmitis, or retrobulbar hemorrhage if the patient complains of pain or vision changes and emergently consult an ophthalmologist.

⯈ Slit-lamp examination, fluorescein staining, and measurement of intraocular pressure are essential elements of a thorough evaluation of the red eye.

⯈ Beware of systemic complications from topical ophthalmologic medications. Allergic reactions and complications such as bronchospasm from topical β-blockers are common.

References

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