CME

Earn Category I CME credit by reading this article and the article beginning on page 18 and successfully
completing the posttest on page 55. 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 December 2010.

Learning objectives
List the elements of the physical examination of a patient with conjunctival inflammation
Review the differential diagnosis of a patient who presents with an acute red eye
Discuss three possible diagnoses that could result in blindness
Describe appropriate treatment for these conditions

Ciliary injection: A differential diagnosis

for the patient with acute red eye
A case report helps to demonstrate how to make an accurate diagnosis in the patient who
presents with this challenging-to-manage ocular manifestation.

he acute red eye is a challenge to diagnose and

manage because this common manifestation
has a wide variety of possible causes. For many
primary care clinicians, the differential diagnosis is confusing and leads to unnecessary referrals or failure to recognize serious pathology. The keys to an
accurate clinical diagnosis of the acute red eye, as with most
other diseases of the body, are to perceptively elicit a history,
make accurate physical observations, and pay careful attention to the profile of the patient in front of you.
This article will not discuss all causes or treatment options for the acute red eye; rather it focuses on ciliary injection, or redness, observed near the limbus. The corneal
limbus is the line of demarcation where the clear corneal
tissue turns into white scleral tissue. Redness of the conjunctiva and sclera that immediately surround the cornea
(or limbus) in a unilateral red eye needs to be recognized
and managed appropriately. The clinical presentation is a
diagnostic dilemma for many primary care and emergency/
urgent care clinicians, who may easily make a wrong diagnosis and initiate the incorrect treatment if important clinical findings are overlooked.

trauma. The patient denied chronic medical problems. Her

family history was negative for any significant eye problems
except that in later years her grandparents had a history of
cataracts. No other family members at home were complaining of similar symptoms.
Physical examination Mrs. B. appeared to be healthy
and in no apparent distress. She was afebrile with lungs
clear to auscultation and had a regular heart rate and
rhythm. She had dark hair, brown eyes, and a dark com-

CASE

Mrs. B., a 32-year-old female, presented to the clinic with a

unilateral, moderately painful, red right eye. Onset of mild
tenderness was 2 days ago, and redness gradually developed
with increasing deep aching pain that the patient described as
a 3 on a 10-point scale (0, no pain; 10, unbearable pain). The
only discharge was mild tearing. The patients medical history was negative for eye problems, and she had no history of
50 JAAPAdecember 201023(12)www.jaapa.com

Iris and lens position

normal position

partially closed angle

closed angle position

Figure 1. Change in iris and lens positions in acute angleclosure glaucoma

Samuel Powdrill, MPhil, PA-C

Samuel Powdrill, MPhil, PA-C

plexion. Her visual acuity was 20/70 OD (the right eye)

and 20/20 OS (the left eye). The patients eyelids were
bilaterally symmetrical and not swollen. Her extraocular
movements were intact. Ciliary injection around a clear
cornea was noted in the patients right eye. The anterior
chamber appeared deep bilaterally without increased iris
shadow. Her pupils were round and reacted to light bilaterally; the pupil of the left eye was slightly larger. Red reflex
was present in both eyes but less bright in the right eye.
The retinas appeared intact and without obvious pathology; however, the retina in the right eye was more difficult
to view. The right cornea did not stain with fluorescein
dye. Intraocular pressure (IOP) on Schiotz tonometry was
approximately 8 mm Hg in the right eye and 14 mm Hg in
the left eye (normal, 10-20 mm Hg).
Laboratory studies The CBC results were within normal
limits, including RBC, 5.13106/L; WBC count, 5,300/L;
platelets, 1523103/L; hemoglobin, 14 g/dL; hematocrit,
42%; and ESR, 10 mm/h. Human leukocyte antigen B27
(HLA-B27) testing was negative.
DISCUSSION

Although conjunctival inflammation in the eyes has a wide

differential diagnosis, the observant clinician can make a
reasonably accurate diagnosis in our patients case. Viral or
bacterial infection must be a consideration but can be ruled
out quickly by the history and physical examination findings.
Most conjunctival viral infections affect both eyes, and the
redness is usually across the entire conjunctiva as well as the
inner surface of the eyelids. The eye typically has a gritty
sensation (the feeling of sand in the eye), burning pain, and
photophobia accompanied by mucous discharge. Bacterial
infection can be unilateral or bilateral, is typically associated
with purulent discharge, and usually involves a history of a
foreign body in the eye or trauma. Corneal ulcer usually produces unilateral conjunctival redness and intense pain. The
ulcer is visible on the cornea with direct light, oblique light,
or fluorescein staining. Frequently, this condition is accompanied by decreased vision.
Our patient had no discharge, mild pain, limited ciliary
injection, no history of trauma, and a clear cornea even with

staining; therefore, infection was very unlikely. Manifestation

as a unilateral red eye with pain suggests that the patient
could have a sight-threatening condition. The three most
likely diagnoses associated with this clinical presentation are
chronic open-angle glaucoma (COAG), acute angle-closure
glaucoma (AACG), and iritis (Table 1).
Chronic open-angle glaucoma should be considered in
this case, but it is not a likely diagnosis. COAG has a very
gradual onset and begins with a mild elevation in intra
ocular pressure (usually 20-40 mm Hg) over a period of
months to years. The iris is in the normal flat position with
a deep anterior chamber and therefore does not create an
iris shadow. Either the flow of aqueous humor to the trabecular meshwork is blocked by a clog of pigment cells, and/
or the transport system that moves fluid in a controlled

Many patients who have chronic

open-angle glaucoma are unaware
of a loss of peripheral vision until
their central vision is affected.
manner through the trabecular meshwork into the Schlemm
canal fails. Risk of developing COAG increases with age,
particularly after age 40 years, and is higher in patients with
a family history of glaucoma.
There is little to no pain or ciliary injection of the conjunctiva until the later stages of disease. Patients who have not had
regular IOP screening may have advanced visual field loss
on presentation because visual field loss progresses from the
periphery inward, eventually producing the classic tunnel
vision. Many patients are not aware of a loss of peripheral
vision until their central vision is affected. Patients with COAG
will usually feel an ache in the eye but may not experience
pain until they have advanced disease. Chronic open-angle
glaucoma usually affects both eyes; however, the disease may
advance more quickly in one eye than in the other.1
Continued on page 52

Key Points
Manifestation as a unilateral red eye with pain suggests that the patient could have a sight-threatening condition. The three most likely

diagnoses associated with this clinical presentation are chronic open-angle glaucoma (COAG), acute angle-closure glaucoma (AACG),
and iritis.
The key features to consider when examining the eye are visual acuity, pain, the area of injection, the cornea, and the pupil. The next
most useful finding is intraocular pressure measurement.
Treatment of glaucoma and iritis are completely opposite from each other. Acute angle-closure glaucoma is treated by constricting the
pupil with pilocarpine eye drops, which draws the iris out of the angle of the eye. Pupil dilation is fundamental to the treatment of iritis.
Verifying that the IOP is not elevated and that the anterior chamber is not shallow before dilating the pupil is essential. Where the
equipment and expertise are not available for either IOP measurement or dilation, referral to an eye specialist is indicated as these
procedures can result in serious damage to the eye when performed by an inexperienced clinician.

www.jaapa.comdecember 201023(12)JAAPA 51

CME Ciliary injection

TABLE 1: Differential diagnosis for Mrs. B.1,3,6
Signs and
symptoms

Chronic open-angle glaucoma

Acute angle-closure glaucoma

Iritis

Visual acuity

Normal central vision until late

stages

Greatly decreased

Slight to significant decrease

Ciliary injection

None or slight

Yes

Yes

Pupil

Mid-dilated (only in advanced

disease)

M
 id-dilated
R
 ound

C
 onstricted
Irregular when dilated

Cornea

Clear unless IOP >35 mm Hg

H
 azy
E
 dematous

Clear or hazy

Intraocular
pressure (normal:
10-20 mm Hg)

Mild to severe elevation

(20-50 mm Hg)

Very high (40-80 mm Hg)

Low or normal

Pain

None to mild headache

S
 evere
O
 ften with nausea

Moderate to severe

Treatment

B
 eta-blocker drops (timolol)
P
 rostaglandin-inhibiting drops

A
 cetazolamide oral (initial dose
of 500 mg, then 125-250 mg
every 4 h)
P
 upil constriction (pilocarpine
drops)
S
 urgery/laser iridectomy

C
 orticosteroid drops
P
 upil dilation (atropine or
homatropine ophthalmic and
phenylephrine drops)

Key: COPD, chronic obstructive pulmonary disease.

Acute angle-closure glaucoma, in contrast, typically

manifests with severe nausea; and unlike chronic openangle glaucoma, AACG produces a very rapid and painful
increase in intraocular pressure. However, the location of
the pain is often poorly defined by the patient, or the patient
complains of abdominal symptoms. This can result in a
missed diagnosis of AACG while the patient is treated for
an abdominal complaint. Measuring visual acuity will demonstrate a rapid decline. In AACG, the anterior chamber
is shallow, and the iris is angled forward so that it blocks
the flow of aqueous humor to the trabecular meshwork
(Figure 1). Because the mechanism of meshwork blockage is
completely different, treatment of AACG is different from
treatment of COAG.
Iritis is often very similar to AACG in appearance. Both
conditions manifest with ciliary injection, the cornea and
anterior chamber are marginally hazy from inflammatory
cells (this finding is suggested by a difficulty in viewing the
retina), and the eye is moderately painful in the early stages
of the condition. However, there are two key differences.
In acute angle-closure glaucoma, the IOP becomes very
high (50-80 mm Hg) rapidly, and in iritis the IOP is usually
somewhat low; however, IOP can be elevated if there are
a lot of inflammatory cells (flare) in the anterior chamber.
The iritic pupil is typically constricted and poorly reactive
to light with posterior adhesions on the lens (synechiae),
which may give the pupil an irregular shape.
The presence of flare in the anterior chamber and keratic precipitates confirm a diagnosis of iritis. Neither of
52 JAAPAdecember 201023(12)www.jaapa.com

these signs can be seen easily with the naked eye. A simple
description of flare is the illusion of light rays shining
through smoke when a pinpoint beam of light is shone
through the anterior chamber. Keratic precipitates are small
yellow or brown particles that can be seen on the inside
surface (endothelium) of the cornea. These arise from the
iris and usually manifest with iritis. Keratic precipitates are

Greater pigmentation in the iris,

skin, and hair is associated with
higher risk of developing chronic
open-angle glaucoma.
visible on direct ophthalmoscopy (+20 diopter lens setting) at 5 cm from the eye. This will give a clear, magnified
view of the cornea and anterior chamber, revealing significant flare, if present. Precipitates can be seen with careful
observation.
MAKING THE DIAGNOSIS

Greater pigmentation in the iris, skin, and hair is associated with the risk of developing COAG. Our patients
brunette hair and dark iris increase the likelihood of the
diagnosis being COAG. However, the history and physical examination findings (unilateral pain, ciliary injection,

TREATMENT

Treatment of glaucoma and iritis are completely opposite

from each other. If the wrong treatment is administered, the
chance of causing blindness in that eye is very high.
Acute angle-closure glaucoma is treated by constricting
the pupil with pilocarpine eye drops, thereby drawing the
iris out of the angle of the eye. When the pupil is dilated,
the iris tissue is stacked up or folded together into the
angle between the cornea and iris. The constriction of the
sphincter muscle around the edge of the pupil pulls the iris
tissue toward the center of the pupil, stretching the tissue
away from the angle. This allows the aqueous fluid to flow
from the posterior chamber into the anterior chamber and
out through the trabecular meshwork and Schlemm canal.
Oral acetazolamide further reduces the IOP by inhibiting
aqueous fluid production, which occurs in the ciliary body.
Intraocular pressure can be reduced surgically by creating a
small hole in the iris with a laser. Resection of a small piece

of iris through a surgical opening in the cornea can also be

used to relieve IOP. Iridectomy can also be performed prophylactically to prevent recurrence or in patients who are at
risk of angle closure.1
Pupil dilation is fundamental to the treatment of iritis.
It is also helpful in the diagnosis, particularly in demonstrating synechiae. These are areas of iris surrounding
the pupil that adhere to the lens and restrict dilation of
the pupil. When dilated, the pupil will have an irregular
appearance much like the petals of a flower.4 Dilation for
diagnostic purposes is done with short-acting mydriatic
drops. Verifying that the IOP is not elevated and that the
anterior chamber is not shallow before dilating the pupil is
essential. Where the equipment and expertise are not available for either IOP measurement or dilation, referral to an
eye specialist is indicated as these procedures can result in
serious damage to the eye when performed by an inexperienced clinician.
After pupil dilation, the synechiae are released. This is
accomplished with strong, longer-acting mydriatics that
both relax the parasympathetic system and stimulate the
sympathetic nervous system. The most commonly used
agents are atropine and phenylephrine. In addition, a topical corticosteroid should be administered to reduce the
inflammatory process. Prednisone 1% drops are usually the
drug of choice, which reduces inflammation and the inflammatory response within the eye.4
Clinicians should note that corticosteroids can make
glaucoma worse. Corticosteroids actually increase fluid
Iritis/uveitis
Light reflex
Pigment
ring from
previous
posterior
synechae
Irregular
pupil with
synechae
Keratic precipitates
Ciliary injection
Scattered light
reflex
Mid-dilated
pupil
Iris shadow
and shallow
interior
chamber
Ciliary injection

Acute angle-closure glaucoma

Figure 2. The differentiation between iritis and acute angleclosure glaucoma
www.jaapa.comdecember 201023(12)JAAPA 53

Samuel Powdrill, MPhil, PA-C; Photos: ISM / Phototake

constricted pupil, low IOP, and rapid onset) do not support this diagnosis.
The most likely cause of this womans red eye is iritis.
The diagnosis rests on the differentiation between acute
angle-closure glaucoma and iritis. Visual acuity is greatly
reduced in patients with AACG; whereas vision loss with
iritis can vary from none to severe if the visual pathways
are involved. Therefore, the key structures to examine are
the area of injection, the cornea, and the pupil2,3 (Figure
2). The location of the injection in our patient is largely
ciliary (around the edge of the cornea/limbus), which
is characteristic of both AACG and iritis. However, in
AACG, the cornea is hazy from corneal edema, and the
pupil is usually mid-dilated and fixed.
The next most useful finding is the intraocular pressure
measurement. When tonometry is not available, a clinical
estimate of IOP can be made with gentle palpation of the
globe through the eyelid. The affected eye can be compared
with the contralateral eye or with the clinicians own eye.
Another clinical sign is an iris shadow, which appears widened in AACG; it indicates a shallow anterior chamber. An
iris shadow will appear across at least a quarter of the medial
side of the iris when a light is shone across the eye from the
lateral side. The shadow is not widened in iritis.
No clear cause is found in 50% of patients with iritis.
Thus an unremarkable history, as in our patients case, is
not surprising. Diseases associated with iritis include arthritis, ankylosing spondylitis, sarcoidosis, and other human
leukocyte antigen B27 (HLA B27) diseases. Erythrocyte
sedimentation rate (ESR) may also be elevated; hence
HLA B27 testing and ESR were performed in our patient.
Tuberculosis or syphilis should be considered even if risk
factors or exposure cannot be confirmed.4 These are two
well-documented causes of iritis and are nearly always
included in the differential diagnosis. Diagnostic testing for
tuberculosis and syphilis is usually performed, especially if
iritis is recurrent and other causes are not found.

CME Ciliary injection

retention and impairment of aqueous drainage, thereby
increasing corneal edema.5 Areas of the iris that adhere to
the lens in iritis will remain adhered after pupil constriction via eye drops. This will result in obscured vision and
requires surgical correction.
Chronic open-angle glaucoma is typically treated with
topical eye drops. The most commonly used agents are
beta-blockers and prostaglandin inhibitors. These medications are given indefinitely as the problem is chronic and
progressive. In advanced or resistant cases of COAG, treatment options are oral medications, laser surgery, or surgical filtration.1
SUMMARY

This case presents the challenge of how to accurately assess

the unilateral painful red eye with ciliary injection. The
diagnosis can be clarified with careful clinical observation
and a few basic clinical tests. Physical examination should
focus on visual acuity; presence of pain; location of redness; shape, size, and reaction of the pupil; and the IOP, if
it can be obtained safely. If a slit lamp is available, the diagnosis can be made more definitively.
Because the diagnosis in a situation like this is usually
made by an eye specialist, a clinical presentation of unilateral painful red eye will normally be referred after an initial

54 JAAPAdecember 201023(12)www.jaapa.com

examination and early management commences. A crucial

role for the physician assistant or other primary care provider is to carefully observe the physical findings, accurately
describe the signs and symptoms, and initiate appropriate
management. These steps will facilitate the referral to an
eye specialist and optimize resolution of these potentially
sight-threatening conditions. JAAPA
Sam Powdrill is an assistant professor in the PA program at the University
of Kentucky, Lexington. The author has indicated no relationships to
disclose relating to the content of this article.
DRUGS MENTIONED
Acetazolamide (Diamox Sequels, generics)
Atropine
Homatropine
Phenylephrine (Cyclomydril)

Pilocarpine (Carpine, Pilopine HS)

Prednisone (Prednisone Intensol, generics)
Timolol (Betimol, Istalol, Timoptic, generics)

REFERENCES
1. Khaw PT, Shah P, Elkington AR. Glaucoma2: treatment. BMJ. 2004;328(7432):156-158.
2. Farina GA, Mazarin GI. Red eye evaluation. eMedicine from WebMD. http://emedicine.medscape.
com/article/1216540-overview. Updated July 30, 2009. Accessed November 2, 2010.
3. Khaw PT, Shah P, Elkington AR. Glaucoma1: diagnosis. BMJ. 2004;328(7431):97-99.
4. Gordon K III. Iritis and uveitis. eMedicine from WebMD. http://emedicine.medscape.com/article/
798323-overview. Updated August 13, 2009. Accessed November 2, 2010.
5. Jones R 3rd, Rhee DJ. Corticosteroid-induced ocular hypertension and glaucoma: a brief review
and update of the literature. Curr Opin Ophthalmol. 2006;17(2):163-167.
6. Riordan-Eva P, Whitcher JP. Vaughan & Asburys General Ophthalmology. 17th ed. New York, NY:
Lange Medical Books/McGraw-Hill; 2008.