Red Eye Case File
[Link]
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.