University of the East

Ramon Magsaysay Memorial Medical Center

COLLEGE OF MEDICINE

Module in Ophthalmology
CASE STUDY 1

RED EYE

Diego is a 27-year-old male, call center agent from Project 7, Quezon City. He came in
at the UERM outpatient clinic for consult because of profuse tearing on his left eye for
the past 2 days.

His condition started 2 days PTC when he noted profuse tearing of his left eye associated
with redness. He also complained of itchiness and has been waking up with difficulty to
open his left eye because of matting of his eyelashes.

Foreign body sensation, glare and burning sensation are some of his related symptoms.
Lately, he also noticed that his right eye is starting to tear profusely and is occasionally
itchy, too. He started to put Visine to no avail of abating his symptoms.

He also mentioned that he has been suffering from colds since 5 days ago, but only
noticed his eye condition 2 days PTC in the office.

He usually works at night until morning and goes out with his friends during his off-days.
He occasionally drinks alcoholic beverages but denies smoking and use of illicit drugs.
He gladly admitted that he is sexually active and goes to girly bars once in a while.
EYE EXAM:

VISION: 20/20 OD EXTRAOCULAR MUSCLES: Full, Unrestricted

20/30+1 OS
J1 OU

DIGITAL TONOMETRY: Soft OU

PUPILS: 3mm round briskly reactive to light

EXTERNAL EYE EXAM: Clinical Findings are noted more on the left eye than the
right eye
Watery mucus discharge, red and edematous eyelids, matted lashes, hyperemic
conjunctiva with some pinpoint subconjunctival hemorrhages, numerous follicles
in the lower cul-de-sac mixed with numerous papillae, a pseudomembrane was
noted on the left. Clear corneas, deep anterior chambers.

VISUAL FIELDS: Full (confrontation)

FUNDUSCOPY: OU
Good Red orange reflex, clear media, delineated disc borders,
Cup-Disk ratio: 0.3, Artreriole-Venule ratio: 2:3, good foveal reflex,
no exudates/hemorrhages.

Other findings: Tender palpable preauricular lymph node, Left.

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DISCUSSION GUIDE:

1. Enumerate the factors to consider in approaching the patient’s case. (Pertinent

Positive and Negative)

2. Give at least 5 conditions that present as a red eye. Differentiate them with
brief comments on their etiology, signs, symptoms, evaluation, management
and prognosis.

3. What is the most probable diagnosis based on the history and P.E.

4. What laboratory/diagnostic tests would you consider? Are these routinely

done?

5. Explain concisely the pathophysiology of the following clinical

findings:hyperemia, chemosis, subconjunctival hemorrhage, discharge,
membrane/pseudomembrane, papillae and follicles.

6. Formulate a rational management plan (treatment and prevention).

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 University of the East
Ramon Magsaysay Memorial Medical Center
COLLEGE OF MEDICINE
Module in Ophthalmology

CASE STUDY 1

RED EYE

TUTOR’S GUIDE

1. Enumerate the factors to consider in approaching the patient’s case. (Pertinent Positive
and Negative)
PERTINENT
Positive Negative
Young, active, healthy (not No history of trauma (mechanical or
immunocompromised) chemical)
Call center agent (occupation – peer Did not instill breastmilk, saliva, urine
pressure) Unknown if co-worker or people around
History of colds/ infection him had the same symptoms
Use of Visine eyedrops Does not use illegal drugs
Sexually Active
Palpable preauricular lymph node

2. Give at least 5 conditions that present as a red eye. Differentiate them with brief
comments on their etiology, signs, symptoms, evaluation, management and prognosis.

5 Entities that may present as a Red Eye:

A. CONJUNCTIVITIS: Infectious or non-infectious inflammation of the

conjunctiva. Etiology: Classically may be allergic, bacterial, chlamydial or
viral in origin. Symptoms may include red eye, swelling, itching, burning,
foreign body sensation, tearing, discharge, crusting of lashes; may have
photophobia and decreased vision. Signs include normal or decreased visual
acuity, lid edema, conjunctival injection, chemosis, papillae, follicles,
membranes, petechial hemorrhages, concretions, discharge; may have
preauricular lymphadenopathy, subepithelial infiltrates, punctate staining,
cornel ulcers, and/or cataract. Evaluation should focus on complete
ophthalmic history and eye exam with attention to preauricular
lymphadenopathy, everting lids, characteristics of discharge, conjunctiva,
cornea, and anterior chamber. Lab tests: consider cultures/smears of
conjunctiva. Management: Treatment depends on etiology; usually
supportive with medications, compresses, and debridement of membranes for
symptomatic relief. Prognosis: usually good; subepithelial infiltrates in
adenoviral conjunctivitis cause variable decreased vision for months.

B. EPISCLERITIS: Sectoral (70%) or diffuse (30%) inflammation of the episclera.

Etiology: idiopathic, tuberculosis, syphilis, herpes zoster, rheumatoid arthritis,
other collagen vascular diseases. Symptoms: Asymptomatic, may have mild
pain and/or red eye. Signs: Subconjunctival and conjunctival injection,
usually sectoral; may have
chemosis, episcleral nodules, anterior chamber cell/flare. Evaluation:
Complete ophthalmic history and eye exam with attention to pattern of
conjunctival and scleral injection and blanching with topical phenylephrine
(scleritis is painful, has a violaceous hue and doe not blanch with topical
vasoconstrictor [phenylephrine 2.5%]), and anterior chamber. Consider
scleritis work-up in recurrent or bilateral cases. Management: No treatment
recommended. Consider limited use of vasoconstrictor (naphazoline-
pheniramine maleate, mild topical steroid, or oral NSAID (indomethacin) if
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 severe. Prognosis: Good; usually self-limited; may be recurrent in 67% of
cases.

C. SCLERITIS: inflammation of the sclera, can be anterior (98%) or posterior

(2%). Etiology: Collagen vascular diseases in 30% of cases (most commonly
rheumatoid arthritis, ankylosing spondylitis, lupus erythematosus, polyarteritis
nodosa, Wegener’s granulomatosis, and relapsing polychondritis); also herpes
zoster, syphilis, tuberculosis, leprosy, gout, porphyria, post-surgical, and
idiopathic. Symptoms: Pain, photophobia, swelling, red eye, decreased vision
(except scleromalacia). Signs: Normal or decreased vision, subconjunctival
and conjunctival injection with violaceous hue, chemosis, scleral edema,
scleral nodule(s), globe tenderness to palpation; may have anterior cell/flare
(30%), corneal infiltrate or thinning, scleral thinning (30%); posterior type
may have chorioretinal folds and/or focal serous retinal detachment.
Evaluation: Complete ophthalmic history and eye exam with attention to
pattern of conjunctival and scleral injection and failure of area to blanch with
topical vasoconstrictor (phenylephrine 2.5%), cornea, anterior chamber. And
ophthalmoscopy. B-scan ultrasonography shows thickened sclera and “T sign”
in posterior scleritis. Lab tests: complete blood count (CBC), rheumatoid
factor (RF), antinuclear antibody (ANA), antineutrophil cytoplasmic antibody
(ANCA), Venereal Disease Research Laboratory (VDRL), fluorescent
treponemal antibody absorption test (FTA-ABS), purified protein derivative
(PPD) and controls, and chest radiographs. Medical consultation.
Management: Depending on severity, consider using one or a combination of
systemic NSAIDs, systemic steroids, H2-blocker and immunosuppressive
agents. May require surgery (patch graft). Prognosis: Depends on etiology;
poor for necrotizing form, which may perforate; scleromalacia perforans
rarely perforates; recurrences common.

D. ACUTE ANGLE-CLOSURE GLAUCOMA: Glaucoma due to obstruction of

trabecular meshwork by peripheral iris; may be primary or secondary, with or
without papillary block. Symptoms: pain, red eye, photophobia,
decreased/blurred vision, haloes around lights, headache, nausea, emesis.
Signs: Decreased visual acuity, increased
intraocular pressure (firm eyeball), ciliary injection, corneal edema, anterior
chamber cell/flare, shallow anterior chamber, narrow angles on gonioscopy,
mid-dilated nonreactive pupil, iris bombé; may have
signs of previous attacks including sector iris atrophy, anterior subcapsular
lens opacities (glaukomflecken), dilated irregular pupil,
and peripheral anterior synechiae (PAS). Evaluation: Complete ophthalmic
history and eye exam with attention to pupils, cornea, tonometry, anterior
chamber, iris, indentation gonioscopy, lens and ophthalmoscopy. Check visual
fields. Management: Topical ß-blockers, alpha agonist, topical steroid,
miotics, systemic acetazolamide and hyperosmotic. Consider laser peripheral
iridotomy. Consider topical cycloplegic in secondary ACG. May require
cataract extraction if lens induced. Prognosis: Good if prompt treatment is
initiated.

E. ANTERIOR UVEITIS (IRITIS, IRIDOCYCLITIS): Inflammation of the anterior

uvea (iris and ciliary body) with exudation of blood cells and protein into the
anterior chamber secondary to breakdown of the blood-aqueous barrier and
increased vascular permeability from a variety of disorders. Etiology: May be
nongranulomatous (lymphocyte and plasma cell infiltrates) or granulomatous
(epithelioid and giant cell infiltrates). Symptoms: pain, photophobia, tearing,
red eye; may have decreased vision. Signs: Normal or decreased visual acuity,
ciliary injection, miosis, anterior chamber cell/flare; may have fine
(nongranulomatous) or mutton-fat (granulomatous) keratic precipitates,
keratitis, iris nodules, increased or decreased intraocular pressure, peripheral
anterior synechiae, posterior synechiae, hypopyon, cataract, vitritis,
retinal/choroidal lesions, cystoid macular edema. Evaluation: Complete
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 ophthalmic history and eye exam with attention to corneal sensation, character
of keratic precipitates, tonometry, anterior chamber, iris, vitreous cells and
ophthalmoscopy. Medical or rheumatology consultation. Management:
Topical steroids, cycloplegics and oral steroids; consider immunomodulating
agents. Prognosis: Depends on etiology; most are benign. Poor if sequelae of
chronic inflammation exist.

F. CORNEAL TRAUMA: Etiology: Chemical/thermal burn, corneal abrasion,

foreign body. Symptoms: pain, foreign body sensation, tearing, red eye and
photophobia. Signs: Normal or decreased visual acuity, conjunctival injection,
ciliary injection, epithelial defects that stain with fluorescein, scleral/limbal
blanching due to ischemia, foreign body, rust ring, corneal edema, anterior
chamber cell/flare. Management: Copious irrigation with fluids, wide-
spectrum topical antibiotic, cycloplegic, , removal of foreign body and rust
ring, Seidel test, bandage contact lens; may have to consider surgery.
Prognosis: Variable; worst for severe alkali burns.

G. INFECTIOUS KERATITIS: Destruction of corneal tissue (epithelium and

stroma) due to inflammation from an infectious organism. Risks include
contact lens wear, trauma, dry eyes, exposure keratopathy,
bullous keratopathy, neurotrophic cornea, and lid abnormalities. Etiology:
bacterial (most common), fungal, parasitic and viral. Symptoms: pain,
decreased corneal sensation, discharge, tearing, photophobia, red eye,
decreased vision; may notice a white spot on the cornea. Signs: Normal or
decreased visual acuity, conjunctival injection, ciliary injection, white corneal
infiltrate with overlying epithelial defect that stains with fluorescein, satellite
lesions (fungal), corneal edema, Descemet’s folds, dendrite (HSV),
pseudodendrite (HZV), cutaneous herpes vesicles, perineural and ring
infiltrates (Acanthamoeba), corneal thinning, descemetocele, anterior chamber
cell/flare, hypopyon, mucopurulent discharge, increased intraocular pressure.
Evaluation: Complete ophthalmic history with attention to contact lens use
and care regimen. Complete eye exam with attention to cornea (sensation, size
and depth of ulcer, character of infiltrate, fluorescein and rose bengal staining,
amount of thinning), tonometry, and anterior chamber. Lab tests: Corneal
scraping stain, culture. May have to consider biopsy. Management: Suspend
use of contact lens, consider bandage contact lens, glue or tarsorrhaphy.
Topical antibiotics, antivirals, topical cycloplegics. May require corneal
transplant. Prognosis: Depends on the organism, size, location and response
to treatment.

3. What is the most probable diagnosis based on the history and P.E.

Most Probable Diagnosis/Etiology: Viral Conjunctivitis

The abrupt onset of unilateral or bilateral red eye, foreign body sensation, and
follicular conjunctival hyperemia often suggests viral conjunctivitis. The vast
majority of cases of viral conjunctivitis are caused by adenovirus. Adenoviral
conjunctivitis is a significant health problem because of the contagiousness of
the disease and an economic problem responsible for numerous working days
lost each year. It typically affects people between the ages of 20 to 40 years
with a slight male preponderance. Epidemic keratoconjunctivitis (EKC),
primarily caused by adenovirus 8, 11, and 18, classically presents with
sudden onset of redness and watery discharge, follicular conjunctivitis and
ipsilaterally tender preauricular lymph node. 7 to 10 days after onset, a
diffuse, punctate subepithelial keratitis may ensue. The fellow eye may
become involved between 2 to 10 days after onset, usually less severely. The
conjunctivitis itself lasts 2 to 3 weeks and is self-limited, but discrete
subepithelial infiltrates may persist for several weeks or months.

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4. What laboratory/diagnostic tests would you consider? Are these routinely done?

Laboratory evaluation: Not routinely done

One may perform GRAMS/GIEMSA staining on conjunctival

swabs/scrapings. Culture/Sensitivity studies may be done. Diagnosis is
usually based on clinical features, and only selected cases are confirmed.
Rapid immunodetection of adenovirus antigen may aid in diagnosis in
confusing cases or epidemic outbreaks. Viral cultures can be performed, but
the cost and time required present obstacles to routine use. The sensitivity of
both types of tests is highest in the first week of acute disease, when viral
shedding is maximal. Immunity: Because more than 30 adenovirus serotypes
exist, acquired immunity to one adenovirus does not prevent infection by
another, accounting for so-called recurrent conjunctivitis.

5. Explain concisely the pathophysiology of the following clinical findings:hyperemia,

chemosis, subconjunctival hemorrhage, discharge, membrane/pseudomembrane, papillae
and follicles.

Red Eye as a Cardinal Sign of Inflammation.

The conjunctiva serves a number of different functions, including secretion of

various tear constituents, providing a structural reservoir for tears, and acting
as a barrier to infectious ocular agents and toxins. Histologically, the
conjunctiva consists of nonkeratinized, stratified squamous epithelium
overlying a highly vascularized, loose connective tissue stroma. The vascular
and lymphatic channels of the conjunctiva form afferent and efferent conduits
for humoral and cellular immune components. The conjunctiva responds to
direct viral invasion or a variety of inflammatory mediators in ways similar to
many other tissues. During bouts of infection, the flow through these channels
is augmented by the action of inflammatory mediators that promote vascular
dilatation, permeability and diapedesis. The cardinal signs of soft tissue
infection (i.e. warmth, redness, and swelling) apply to the
conjunctiva as well. Certain clinical signs may be very helpful in narrowing
the differential diagnosis and focusing therapy.

The most common sign of conjunctival inflammation is hyperemia. The

conjunctival vessels become dilated causing an erythematous appearance.
Dilation of the external ocular blood vessels is customarily divided into ciliary
and conjunctival injection. Ciliary injection involves branches of the anterior
ciliary arteries that become congested in inflammation of the cornea, iris and
ciliary body and angle closure glaucoma. They are found near the
corneoscleral limbus and fade towards the fornix. Conjunctival injection
affects mainly the posterior conjunctival blood vessels that extend from the
peripheral marginal arcade in the eyelid and anastomose with the anterior
ciliary arteries at the limbus. They are most numerous at the conjunctival
fornix and are congested in conjunctival inflammations.

Conjunctival hyperemia causes a slight increase in temperature due to

increased blood flow. The minor increase in temperature is thought to promote
growth of microorganisms but also enhances the activity of local defense
mechanisms. Increased temperature may also promote reepithelialization and
wound healing.

Edema in the form of chemosis, with or without subconjunctival

hemorrhage, may also be present and is due to increased vascular
permeability and damage to conjunctival vessels.
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 A discharge may also be present depending on the severity of the infection.
The discharge may present as a simple increase in tear production with
epiphora; as a clear mucous catarrhal discharge; or as a thick, frankly purulent
discharge (superimposed bacterial infection).

Exudate is also, in part, a result of transudation of fluid from increased

vascular permeability. Exudate contains neutrophils and cellular debris. Most
viral infections tend to cause a watery discharge, while bacterial infections
tend to cause a mucous or mucopurulent discharge. Conjunctival
inflammation may also cause membrane or pseudomembrane production.
These appear as a glistening coating of the conjunctival surface, usually in the
inferior cul-de-sac. True membranes cannot be removed from the conjunctival
surface without bleeding of the underlying tissue. A pseudomembrane may be
removed with minimal disturbance of the tissue beneath it. Histologically,
membranes and pseudomembranes are simply different degrees of the same
process. Fibrin and other serum constituents may
form a coagulum on the conjunctival surface. This coagulum also contains
numerous necrotic conjunctival epithelial cells and inflammatory cells.
Membranes may be seen in viral, bacterial, or allergic forms of conjunctivitis
and also after a chemical burn.

Several signs of inflammation are specific to the conjunctiva. One of the more
specific signs is papillary hypertrophy. Papillae are small. Polygonal
elevations of the conjunctival surface usually much less than 1 mm in
diameter. They give a velvety red appearance to the palpebral conjunctiva.
Histologically, papillae are collections of heaped-up inflammatory cells with a
central fibrovascular core attached to the
tarsal plate. Small papillae are a nonspecific finding of conjunctival
inflammation and do not suggest any particular diagnosis.

Conjunctival follicles are another special manifestation of conjunctival

inflammation. Follicles appear as smooth, yellow-white elevations of the
palpebral or limbal conjunctiva. Vessels may be seen around the surface but
not within these elevations. Clinically, follicles give a pebbly appearance to
the conjunctiva, which can be enhanced by instilling fluorescein into the eye.
The fluorescein will pool at the base of the follicles. Histologically, follicles
are aggregations of lymphocytes in the form of germinal centers located in the
conjunctival stroma. The presence of follicles can narrow the differential
diagnosis of conjunctivitis considerably. Certain types of conjunctivitis are
much more likely to stimulate follicle formation than others. These include
adenoviral, primary herpetic, adult inclusion, trachoma, molluscum, and
certain drug-induced forms of conjunctivitis.

6. Formulate a rational management plan (treatment and prevention).

Management

Treatment: Currently no effective therapy for adenovirus EKC. Therapy is

mainly supportive and centers on symptomatic treatment of the foreign body
sensation and irritation through sunglasses or goggles to decrease
photophobia, topical decongestants/antihistamine (naphazoline/pheniramine
eyedrops), cool compresses and artificial tears. Topical antibiotics are given
for superimposed bacterial infection. Peeling of pseudomembranes or
membranes and mild topical steroids may be used.

Prevention: Viral conjunctivitis is very contagious, usually for 10 – 12 days

from the day of onset. Epidemic adenovirus conjunctivitis, which develops
after exogenous contact with infected secretions, can be spread by eye-to-
hand contact or by intermediary contact with a contaminated surface, or
fomite, such as a tonometer tip (incubation period: 5-12 days). Patients with
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external ocular adenovirus infections should be informed of the natural course
of the disease to allay anxiety they may experience if severe conjunctival
chemosis or eyelid edema develops. Any medical personnel harboring
epidemic keratoconjunctivitis should be quarantined for at least 2 weeks to
minimize the infectious spread of the virus. Any patient with adenovirus EKC
should refrain from working in public and remain home for 2 weeks after the
diagnosis is confirmed. They should avoid touching their eyes, shaking hands
with other people, sharing towels and other similar behavior. As long as the
eye is red or weeping he should not attend school. If a patient must work to
avoid tremendous economic difficulties, strict quarantine requirements
including isolation, hand washing and the use of gloves, goggles, mask to
prevent dissemination are imperative. If a patient is quarantined, family
members are instructed to use separate hand towels, washrags, and
pillowcases to prevent dissemination at home. The patient is advised to use
disposable tissue instead of a hand towel.