Fiction reveals truths that reality obscures.

Redness is the most frequently encountered symptom of
ocular disorders. It is due to hyperemia of the conjunctival,
episcleral, or ciliary vessels; erythema of the eyelids; or
subconjunctival hemorrhage. The major differential diagnoses are
conjunctivitis, corneal disorders, acute glaucoma, and acute uveitis (Table 7-1).

Ocular pain may be caused by trauma, infection, inflammation, or sudden increase in intraocular pressure.

Foreign body sensation may
be due to corneal or conjunctival foreign bodies, disturbance of the
corneal epithelium, or rubbing of eyelashes against the cornea
(trichiasis).

Photophobia is usually due
to corneal inflammation (keratitis) or iritis. Other causes are
albinism, aniridia, cone dystrophy, aphakia, or fever associated with
various systemic infections.

Itching is characteristically associated with allergic eye disease.

Scratching and burning due
to dryness of the eyes may be due to dry environment, ocular surface
disease, systemic disorders (eg, Sjögren’s disease), or drugs (eg,
atropine-like agents).

Watering is usually due to
inadequate tear drainage through obstruction of the lacrimal drainage
system or malposition of the lower lid. Reflex tearing occurs with any
disturbance of the corneal epithelium.

Eyestrain is discomfort associated with prolonged
reading or close work. Refractive error including presbyopia,
inadequate illumination, and latent ocular deviation are the usual
causes. Headache is rarely due to ocular disorders but is a major
symptom of giant cell arteritis, an important cause of visual loss in
older individuals.

Purulent discharge usually indicates bacterial infection
of the conjunctiva, cornea, or lacrimal sac. Viral conjunctivitis or
keratitis produces watery discharge; allergic conjunctivitis results in
tearing, ropy discharge, and itching.

Causes of blurred vision include refractive error,
cataract, macular degeneration, diabetic retinopathy, vitreous
hemorrhage, retinal detachment involving the macula, central retinal
vein occlusion, central retinal artery occlusion, intraocular
inflammation (uveitis), corneal opacities, and optic nerve disorders.

Monocular field loss usually indicates disease of the
retina or optic nerve. Important causes are chronic glaucoma, retinal
detachment, branch retinal artery or vein occlusion, optic neuritis,
and anterior ischemic optic neuropathy, all of which, especially
chronic glaucoma, may be bilateral. Lesions of the optic chiasm due to
pituitary tumors usually result in bitemporal field loss. Retrochiasmal
lesions cause contralateral homonymous field defects. The more
posterior the lesion in the visual pathway, the more similar are the
defects in the two eyes. Cerebrovascular disease and tumors are
responsible for most lesions of the retrochiasmal visual pathways.

An individual is visually impaired if best corrected
distant visual acuity in the better eye is 20/80 or less or if visual
fields are significantly restricted. Legal blindness is defined as
visual acuity for distant vision of 20/200 or less in the better eye
with best correction or widest diameter of the visual field subtending
an angle of less than 20. Most states require best corrected visual
acuity with both eyes of 20/40 for an unrestricted driving license.

The World Health Organization (WHO) estimates that of
the world’s population over 160 million people are visually impaired
and about 37 million are blind. The most frequent causes of blindness
worldwide are cataract, glaucoma, age-related macular degeneration, and
diabetic retinopathy, all of which are increasing in prevalence,
especially in older individuals, as well as

trachoma. In the United States, over 3 million adults aged 40 years or over are blind or visually impaired.

Double vision typically results from acquired ocular
misalignment. This may be caused by central disorders of eye movements
or cranial nerve palsies due to head injury, vascular, neoplastic, or
inflammatory intracranial disease, or Wernicke’s syndrome; myasthenia
gravis; or intraorbital lesions including Graves’ ophthalmopathy and
muscle entrapment as a result of orbital blowout fracture. Monocular
diplopia, which persists when the fellow eye is covered, is usually due
to refractive error or lens opacities.

Spots before the eyes (floaters) are often caused by
benign vitreous opacities. However, they may also be caused by
posterior vitreous detachment, vitreous hemorrhage, or posterior
uveitis. Sudden onset of floaters, particularly when associated with
flashing lights (photopsia), necessitates dilated fundal examination to
exclude a retinal tear or detachment.

Corrected distant visual acuity should be tested for
each eye in turn, using a Snellen or logMAR (EDTRS) chart, annotated
according to the distance at which each line can be read by a normal
individual. It is traditionally measured at 20 feet (6 meters in
Europe) or nearer if vision is poor, but other test distances may be
used. Visual acuity is expressed as a fraction—the test distance over
the figure assigned to the lowest line the patient can read. If the
patient is unable to read the top line of the chart, acuity is recorded
as counting fingers (CF), hand movements (HM), perception of light
(LP), or no light perception (NLP). A corrected acuity of less than
20/30 (6/9) is abnormal.

Near acuity is tested with a reduced Snellen chart or
standardized reading test types. The patient must be wearing
appropriate reading correction.

Confrontation testing, preferably using a 5-mm red
target, is valuable for rapid assessment of field defects. Amsler
charts are the easiest method of detecting central field abnormalities
due to macular disease.

The pupils are examined for absolute and relative size
and reactions to both light and accommodation. A large, poorly reacting
pupil may be due to third nerve palsy, iris damage caused by acute
glaucoma, or pharmacologic mydriasis. A small, poorly reacting pupil is
observed in Horner’s syndrome, inflammatory adhesions between iris and
lens (posterior synechiae), or neurosyphilis (Argyll Robertson pupils).
Physiologic anisocoria is a common cause of unequal pupils that react
normally.

A relative afferent pupillary defect, in which the
pupillary light reaction is reduced when light is shined into the
affected eye compared with the normal eye, generally indicates optic
nerve disease. It is detected with the “swinging light test,” in which
the pupillary light reactions are compared as a bright light is moved
from one eye to the other.

Examination of extraocular movements begins with an
assessment of whether the two eyes are correctly aligned. A
misalignment of the visual axes under binocular viewing conditions is
known as a manifest deviation, or tropia. A deviation when binocular function is disrupted is known as a latent deviation, or phoria.
A manifest deviation may be apparent by comparing the relative
positions of the corneal light reflexes. A more reliable test is the cover test,
in which the deviated eye moves to take up fixation when the other eye
is occluded. The correctional movement is in the direction opposite to
that of the original manifest deviation. If no manifest deviation is
present, occlusion of one eye will elicit any latent deviation because
binocular function will have been disrupted. As the occluder is removed
(uncover test), latent deviation is then
detected by any correctional movement that occurs to reestablish the
normal alignment of the eyes. Latent deviation is common among normal
individuals.

Horizontal diplopia indicates dysfunction of the medial
and lateral rectus muscles; vertical diplopia results from dysfunction
of the superior or inferior recti or the obliques. The false outer
image arises from the affected eye. If muscle contraction is impaired,
the image separation will be greatest in its normal direction of
action; if a muscle cannot relax, image separation will be greatest in
the direction opposite to its normal action. For example, a paretic
lateral rectus or a tethered medial rectus of the right eye will cause
maximal image separation on looking to the right.

Nystagmus in the primary position is always abnormal.
Minor degrees of nystagmus at the extremes of gaze are normal. Other
forms of physiologic nystagmus include optokinetic nystagmus and
nystagmus induced by rotation or caloric stimulation. Exaggerated
gaze-evoked nystagmus may be due to drugs or posterior fossa disease.

Proptosis is suspected when there is widening of the palpebral aperture, with exposure of sclera both superiorly

and inferiorly. (Eyelid retraction causes more exposure superiorly than
inferiorly.) By viewing from above while the patient is asked to look
down and the upper lids are lifted by the examiner, a further estimate
of the degree of proptosis can be made. Exophthalmometry provides
objective assessment. In nonaxial proptosis, there is also horizontal
or vertical displacement of the globe, indicating the presence of a
mass lesion outside the extraocular muscle cone.

The most frequent cause of proptosis in adults is
dysthyroid eye disease. Other causes include cellulitis, tumors, and
orbital pseudotumor.

Ptosis is usually due to eyelid disease. Neurologic
causes of ptosis include Horner’s syndrome, in which the pupil is
constricted, and third nerve palsy, in which there are abnormalities of
eye movements and the pupil may be dilated and react poorly to light.
In myasthenia gravis, the pupils are normal and characteristically the
ptosis is fatiguable.

Although slit-lamp examination is more sensitive,
examination with a flashlight and loupe usually provides sufficient
information for initial assessment. Patterns of redness indicate the
site of the problem. In conjunctivitis, it extends diffusely across the
globe and the inner surface of the lids. Keratitis, intraocular
inflammation, and acute glaucoma lead to predominantly circumcorneal
injection. Episcleritis and scleritis cause localized or diffuse deep
injection, which in the case of scleritis is associated with blue
discoloration.

Focal lesions of the cornea due to infection or trauma
can be differentiated from the diffuse corneal haze of acute glaucoma
and from the cloudiness of the anterior chamber and perhaps hypopyon
(white cells within the anterior chamber) of iritis. Instillation of
fluorescein and examination with a blue light aid in detection of
corneal epithelial defects.

Direct ophthalmoscopy, ideally following pupil dilation
with tropicamide 0.5–1%, which rarely induces angle-closure glaucoma,
is used for examining the retina. Assessment of the red reflex and
clarity of fundal details indicate the degree of media opacity.
Abnormalities may then be localized to the cornea, lens, or vitreous by
variations of focus of the ophthalmoscope and use of parallax.

The optic disk is examined for swelling, pallor, and
glaucomatous cupping. Macular lesions causing poor central vision are
usually apparent. The retinal vessels are scrutinized for caliber and
wall changes. Retinal hemorrhages, exudates, and cotton-wool spots are
noted. In hospital patients, dilation should be noted in the record to
avoid confusion on neurologic examination.

Contact lenses are used mostly for correction of
refractive errors, for which they often provide a better optical
correction than glasses, as well as for management of diseases of the
cornea, conjunctiva, or lids. The various types are hard lenses, rigid
gas-permeable lenses, and soft lenses. Hard lenses are much more
durable and easier to care for than soft lenses but are more difficult
to tolerate. Rigid gas-permeable lenses are an effective compromise.

Contact lens care includes cleaning and sterilization
whenever the lenses are removed and removal of protein deposits as
required. Sterilization is accomplished by thermal or chemical methods.
For individuals developing reactions to preservatives in contact lens
solutions, preservative-free systems are available. All contact lenses
can be inserted in the morning and removed at night. Soft lenses are
also available for extended wear. Disposable soft lenses to avoid the
necessity for lens cleaning and sterilization are available for daily
or extended wear.

The major risk from contact lens wear is corneal
ulceration, potentially a blinding condition. Soft lenses present the
major hazard, particularly with extended wear, for which there is an
approximately eightfold increase in risk of corneal ulceration compared
with daily wear. The increased risk from extended wear begins with the
first night of overnight wear and increases progressively thereafter.
Disposable lenses are also associated with corneal ulceration.

Contact lens wearers should be made aware of the risks
they face and ways to minimize them, such as avoiding extended-wear
soft lenses and maintaining meticulous lens hygiene, including not
using tap water for lens cleaning. Whenever there is ocular discomfort
or redness, contact lenses should be removed. Ophthalmologic care
should be sought if symptoms persist.

Hordeolum is a common staphylococcal abscess that is
characterized by a localized red, swollen, acutely tender area on the
upper or lower lid. Internal hordeolum is a meibomian gland abscess
that points onto the conjunctival surface of the lid; external
hordeolum or sty is smaller and on the margin.

Warm compresses are helpful. Incision may be indicated
if resolution does not begin within 48 hours. An antibiotic ointment
(bacitracin or erythromycin) applied to the eyelid every 3 hours may be
beneficial during the acute stage. Internal hordeolum may lead to
generalized cellulitis of the lid.

Chalazion is a common granulomatous inflammation of a
meibomian gland that may follow an internal hordeolum. It is
characterized by a hard, nontender swelling on the upper or lower lid
with redness and swelling of the adjacent conjunctiva. If the chalazion
is large enough to impress the cornea, vision will be distorted.
Treatment is by incision and curettage.

Verrucae and papillomas of the skin of the lids can
often be excised by the general physician if they do not involve the
lid margin; otherwise, surgery should be performed by an
ophthalmologist so as to avoid permanent notching of the lid. Basal
cell epithelioma, squamous cell carcinoma, meibomian gland carcinoma,
and malignant melanoma should be excluded by microscopic examination of
the excised material since 2% of lesions thought to be benign
clinically are found to be malignant. Basal cell epithelioma

is
the most common of these lesions. Mohs’ technique of intraoperative
examination of excised tissue is particularly valuable in ensuring
complete excision of eyelid tumors.

Blepharitis is a common chronic bilateral inflammatory
condition of the lid margins. Anterior blepharitis involves the eyelid
skin, eyelashes, and associated glands. It may be ulcerative, because
of infection by staphylococci, or seborrheic dermatitis, and associated
with seborrhea of the scalp, brows, and ears. Both types may be
present. Posterior blepharitis results from inflammation of the
meibomian glands. There may be bacterial infection, particularly with
staphylococci, or primary glandular dysfunction, in which there is a
strong association with acne rosacea.

Symptoms of blepharitis are irritation, burning, and
itching. In anterior blepharitis, the eyes are “redrimmed,” and scales
or granulations can be seen clinging to the lashes. In posterior
blepharitis, the lid margins are hyperemic with telangiectasias; the
meibomian glands and their orifices are inflamed, with dilation of the
glands, plugging of the orifices, and abnormal secretions. The lid
margin is frequently rolled inward to produce a mild entropion, and the
tears may be frothy or abnormally greasy.

Blepharitis is a common cause of recurrent
conjunctivitis. Both anterior and, more particularly, posterior
blepharitis may be complicated by hordeola or chalazions; abnormal lid
or lash positions, producing trichiasis; epithelial keratitis of the
lower third of the cornea; marginal corneal infiltrates; and inferior
corneal vascularization and thinning.

In anterior blepharitis, cleanliness of the scalp,
eyebrows, and lid margins is effective local therapy. Scales must be
removed from the lids daily with a damp cotton applicator and baby
shampoo. An antistaphylococcal antibiotic eye ointment such as
bacitracin or erythromycin is applied daily to the lid margins with a
cotton-tipped applicator. Antibiotic sensitivity studies may be
required in severe staphylococcal blepharitis.

In mild posterior blepharitis, regular meibomian gland
expression may be sufficient to control symptoms. Inflammation of the
conjunctiva and cornea indicates a need for more active treatment,
including long-term low-dose systemic antibiotic therapy, usually with
tetracycline (250 mg twice daily), doxycycline (100 mg daily),
minocycline (50–100 mg daily) or erythromycin (250 mg three times
daily), and short-term topical steroids, eg, prednisolone, 0.125% twice
daily. Topical therapy with antibiotics such as ciprofloxacin 0.3%
ophthalmic solution twice daily may be helpful but should be restricted
to short courses.

Entropion (inward turning of usually the lower lid)
occurs occasionally in older people as a result of degeneration of the
lid fascia, or may follow extensive scarring of the conjunctiva and
tarsus. Surgery is indicated if the lashes rub on the cornea. Botulinum
toxin injections may also be used for temporary correction of the
involutional lower eyelid entropion of older people.

Ectropion (outward turning of the lower lid) is common
with advanced age. Surgery is indicated if there is excessive tearing,
exposure keratitis, or a cosmetic problem.

Dacryocystitis is infection of the lacrimal sac due to
obstruction of the nasolacrimal system. It may be acute or chronic and
occurs most often in infants and in persons over 40 years. It is
usually unilateral.

The usual infectious organisms are Staphylococcus aureus and β-hemolytic streptococci in acute dacryocystitis and S epidermidis, anaerobic streptococci, or Candida albicans in chronic dacryocystitis.

Acute dacryocystitis is characterized by pain, swelling,
tenderness, and redness in the tear sac area; purulent material may be
expressed. In chronic dacryocystitis, tearing and discharge are the
principal signs, and mucus or pus may also be expressed.

Acute dacryocystitis responds well to systemic
antibiotic therapy. Surgical relief of the underlying obstruction is
usually undertaken electively but may be performed acutely. The chronic
form may be kept latent with antibiotics, but relief of the obstruction
is the only cure. In adults, the standard procedure for obstruction of
the lacrimal drainage system is dacryocystorhinostomy, which involves
surgical exploration of the lacrimal sac and formation of a fistula
into the nasal cavity. Laser-assisted endoscopic dacryocystorhinostomy
and balloon dilation or probing of the nasolacrimal system are
alternatives. Congenital nasolacrimal duct obstruction often resolves
spontaneously but if necessary can be treated by probing of the
nasolacrimal system.

The organisms isolated most commonly in bacterial conjunctivitis are staphylococci, streptococci (particularly S pneumoniae), Haemophilus species, Pseudomonas, and Moraxella.
All may produce a copious purulent discharge. There is no blurring of
vision and only mild discomfort. In severe cases, examination of
stained conjunctival scrapings and cultures is recommended.

The disease is usually self-limited, lasting about 10–14
days if untreated. A sulfonamide (eg, sulfacetamide, 10% ophthalmic
solution or ointment) instilled locally three times daily will usually
clear the infection in 2–3 days. Povidone-iodine may also be effective.
The use of topical fluoroquinolones is rarely justified for treatment
of a generally self-limiting, benign infection.

One of the most common causes of viral conjunctivitis is
adenovirus type 3. Conjunctivitis due to this agent is usually
associated with pharyngitis, fever, malaise, and preauricular
adenopathy (pharyngoconjunctival fever). Locally, the palpebral
conjunctiva is red, and there is a copious watery discharge and scanty
exudate. Children are more often affected than adults, and contaminated
swimming pools are sometimes the source of infection. The disease
usually lasts 10 days.

Epidemic keratoconjunctivitis is caused by adenovirus
types 8, 19, 29, and 37. It is more likely to be complicated by visual
loss due to corneal subepithelial infiltrates. The disease lasts at
least 2 weeks. Local sulfonamide therapy prevents secondary bacterial
infection and cold compresses reduce the discomfort of the associated
lid edema.

This is a common disorder, particularly in elderly
women. A wide range of conditions predispose to or are characterized by
dry eyes. Hypofunction of the lacrimal glands, causing loss of the
aqueous component of tears, may be due to aging, hereditary disorders,
systemic disease (eg, Sjögren’s syndrome), or systemic and topical
drugs. Excessive evaporation of tears may be due to environmental
factors (eg, a hot, dry, or windy climate) or abnormalities of the
lipid component of the tear film, as in blepharitis. Mucin deficiency
may be due to malnutrition, infection, burns, or drugs. Hormone
replacement therapy may increase the risk of dry eyes.

The patient complains of dryness, redness, or a scratchy
feeling of the eyes. In severe cases there is persistent marked
discomfort, with photophobia, difficulty in moving the eyelids, and
often excessive mucus secretion. In many cases, inspection reveals no
abnormality, but on slitlamp examination there are subtle abnormalities
of tear film stability and reduced volume of the tear film meniscus
along the lower lid. In more severe cases, damaged corneal and
conjunctival cells stain with 1% rose bengal, which is to be avoided in
severe cases because of the intense pain. In the most severe cases
there is marked conjunctival injection, loss of the normal conjunctival

and
corneal luster, epithelial keratitis that may progress to frank
ulceration, and mucous strands. Schirmer’s test, which measures the
rate of production of the aqueous component of tears, may be helpful,
but false-positive and false-negative results are frequent.

Treatment depends upon cause. In most early cases, the
corneal and conjunctival epithelial changes are reversible. Aqueous
deficiency can be treated by replacement of the aqueous component of
tears with various types of artificial tears. The simplest preparations
are physiologic (0.9%) or hypo-osmotic (0.45%) solutions of sodium
chloride. Balanced salt solution is more physiologic but also more
expensive. All of these drop preparations can be used as frequently as
every half-hour, but in most cases are needed only three or four times
a day. More prolonged duration of action can be achieved with drop
preparations containing methylcellulose (eg, Isopto Plain) or polyvinyl
alcohol (eg, Liquifilm Tears or HypoTears), or by using petrolatum
ointment (Lacri-Lube). Such mucomimetics are particularly indicated
when there is mucin deficiency. If there is tenacious mucus, mucolytic
agents (eg, acetylcysteine, 20% six times daily) may be helpful. The
presence of ocular surface and lacrimal gland inflammation in dry eyes
has prompted trials of topical antiinflammatory agents such as
cyclosporin A.

Lacrimal punctal occlusion by canalicular plugs or
surgery is useful in severe cases. Blepharitis is treated as described
above. Associated blepharospasm responds to botulinum toxin injections.

Artificial tear preparations are generally very safe and
without side effects. However, the preservatives necessary to maintain
their sterility are potentially toxic and allergenic and may cause
keratitis and cicatrizing conjunctivitis in frequent users.
Furthermore, the development of such reactions may be misinterpreted by
both the patient and the doctor as a worsening of the dry eye state
requiring more frequent use of the artificial tears and leading in turn
to further deterioration, rather than being recognized as a need to
change to a preservative-free preparation.

Allergic eye disease takes a number of different forms
but all are expressions of atopy, which may also manifest as atopic
asthma, atopic dermatitis, or allergic rhinitis. Symptoms include
itching, tearing, redness, stringy discharge, and, occasionally,
photophobia and visual loss.

Allergic conjunctivitis is a benign disease, occurring
usually in late childhood and early adulthood. It may be seasonal,
developing usually during the spring or summer, or perennial. Clinical
signs are limited to conjunctival hyperemia and edema (chemosis), the
latter at times being marked and sudden in onset. Vernal
keratoconjunctivitis also tends to occur in late childhood and early
adulthood. It is usually seasonal, with a predilection for the spring.
Large “cobblestone” papillae are noted on the upper tarsal conjunctiva.
There may be lymphoid follicles at the limbus. Atopic
keratoconjunctivitis is a more chronic disorder of adulthood. Both the
upper and the lower tarsal conjunctivas exhibit a fine papillary
conjunctivitis with fibrosis, resulting in forniceal shortening and
entropion with trichiasis. Staphylococcal blepharitis is a complicating
factor. Corneal involvement, including refractory ulceration, is
frequent during exacerbations of both vernal and atopic
keratoconjunctivitis. They may also be complicated by herpes simplex
keratitis.

For mild and moderately severe allergic eye disease, a topical histamine H₁-receptor
antagonist, such as levocabastine hydrochloride 0.05% or emedastine
difumarate 0.05%, or ketorolac tromethamine, a nonsteroidal
anti-inflammatory agent, is applied topically four times daily.
Ketotifen 0.025%, which has histamine H₁-receptor
antagonist, mast cell stabilizer, and eosinophil inhibitor activity, is
applied two to four times daily; olopatadine 0.1%, applied twice daily,
reduces symptoms by a similar mechanism. Topical mast cell stabilizers,
such as cromolyn sodium 4% or lodoxamide tromethamine 0.1%, applied
four times daily, or nedocromil sodium 2%, applied twice daily, produce
longer-term prophylaxis but the therapeutic response may be delayed.
Topical vasoconstrictors and antihistamines are advocated in hay fever
conjunctivitis but are of limited efficacy and may produce rebound
hyperemia and follicular conjunctivitis. Systemic antihistamines may be
useful in prolonged atopic keratoconjunctivitis. Topical
corticosteroids are essential to the control of acute exacerbations of
both vernal and atopic keratoconjunctivitis. Steroid-induced side
effects, including cataracts, glaucoma, and exacerbation of herpes
simplex keratitis, are major problems. Topical cyclosporin may be
effective. Systemic steroid therapy and even plasmapheresis may be
required in severe atopic keratoconjunctivitis. In allergic
conjunctivitis, specific allergens may be identifiable and thus
avoidable. In vernal keratoconjunctivitis, a cooler climate often
provides significant benefit.

Bacterial keratitis pursues an aggressive course.
Precipitating factors include contact lens wear—especially soft contact
lenses worn overnight—and corneal trauma, including laser surgery. The
pathogens most commonly isolated are Pseudomonas aeruginosa, Pneumococcus, Moraxella
species, and staphylococci. The cornea is hazy, with a central ulcer
and adjacent stromal abscess. Hypopyon is often present. The ulcer is
scraped to recover material for Gram stain and culture prior to
starting treatment with high-concentration topical antibiotics applied
hourly day and night for at least the first 24 hours. Fluoroquinolones
such as ciprofloxacin 0.3%, ofloxacin 0.3%, and norfloxacin 0.3% are
commonly used as first-line agents. Experience with levofloxacin 0.5%,
which is more effective against pneumococci than ciprofloxacin, and the
fourth-generation fluoroquinolones (moxifloxacin 0.5% and gatifloxacin
0.3%), which are active against mycobacteria, is limited. Gram-positive
cocci can also be treated with a cephalosporin such as cefazolin, 100
mg/mL; and gram-negative bacilli with an aminoglycoside such as
tobramycin, 15 mg/mL. If no organisms are seen, these two agents can be
used together.

Herpes simplex keratitis is an important cause of ocular
morbidity in adults. The ability of the virus to colonize the
trigeminal ganglion leads to recurrences precipitated by fever,
excessive exposure to sunlight, or immunodeficiency.

The dendritic (branching) ulcer is the most
characteristic manifestation of this epithelial keratitis. More
extensive (“geographic”) ulcers also occur, particularly if topical
corticosteroids have been used. These ulcers are most easily seen after
instillation of fluorescein and examination with a blue light.
Epithelial disease in itself does not lead to corneal scarring. It
responds well to simple debridement and patching. More rapid healing
can be achieved by the addition of topical antivirals such as
trifluridine drops, vidarabine ointment, acyclovir ointment, or
ganciclovir gel. Long-term oral acyclovir reduces the rate of recurrent
epithelial disease, for which topical corticosteroids must not be used.

Stromal herpes simplex keratitis produces increasingly
severe corneal opacity with each recurrence. Topical antivirals alone
are insufficient to control stromal disease. Thus, topical
corticosteroids are used in combination, but steroid dependence is a
common consequence. Corticosteroids may also enhance viral replication,
exacerbating epithelial disease. Oral acyclovir, 200–400 mg five times
a day, may be helpful in the treatment of severe herpetic keratitis and
for prophylaxis against recurrences, particularly in atopic or
HIV-infected individuals. Corneal grafting is necessitated by severe
stromal scarring, but the overall outcome is relatively poor. Caution:
For patients with known or possible herpetic disease, topical
corticosteroids should be prescribed only with ophthalmologic
supervision.

Fungal keratitis tends to occur after corneal injury
involving plant material or in an agricultural setting, in eyes with
chronic ocular surface disease, and in contact lens wearers. It is an
indolent process, with the cornea characteristically having multiple
stromal abscesses and relatively little epithelial loss. Intraocular
infection

is
common. Corneal scrapings are cultured on media suitable for fungi
whenever the history or corneal appearance is suggestive of fungal
disease.

Acanthamoeba is an important cause of suppurative
keratitis in contact lens wearers. Although severe pain with perineural
and ring infiltrates in the corneal stroma is characteristic, earlier
forms with changes confined to the corneal epithelium are identifiable.
Culture requires specialized media. Treatment is hampered by the
organism’s ability to encyst within the corneal stroma. Various agents
have been used, including neomycin-polymyxin-gramicidin, chlorhexidine,
the investigational agents propamidine isethionate and polyhexamethyl
biguanide, and oral and topical imidazoles such as ketoconazole,
miconazole, and itraconazole. Epithelial debridement may be useful in
early infections. Corneal grafting may be required in the acute stage
to arrest the progression of infection or after resolution to restore
vision. Systemic immunosuppression may be needed if there is scleral
involvement.

Herpes zoster frequently involves the ophthalmic
division of the trigeminal nerve. It presents with malaise, fever,
headache, and periorbital burning and itching. These symptoms may
precede the eruption by a day or more. The rash is initially vesicular,
quickly becoming pustular and then crusting. Involvement of the tip of
the nose or the lid margins predicts involvement of the eye. Ocular
signs include conjunctivitis, keratitis, episcleritis, and anterior
uveitis, often with elevated intraocular pressure. Recurrent anterior
segment inflammation, neurotrophic keratitis, and posterior subcapsular
cataract are long-term complications. Optic neuropathy, cranial nerve
palsies, acute retinal necrosis, and cerebral angiitis are infrequent
problems in the acute stage. HIV infection is an important risk factor
for herpes zoster ophthalmicus and increases the likelihood of
complications.

High-dose oral acyclovir (800 mg five times a day),
valacyclovir (1 g three times a day), or famciclovir (250–500 mg three
times a day) started within 72 hours after the appearance of the rash
reduces the incidence of ocular complications but not of postherpetic
neuralgia. Anterior uveitis requires treatment with topical
corticosteroids and cycloplegics. Neurotrophic keratitis is an
important cause of long-term morbidity.

Primary acute angle-closure glaucoma occurs only with
closure of a preexisting narrow anterior chamber angle, found in
elderly persons (owing to enlargement of the lens), hyperopes, and
Asians. In the United States, about 1% of people over age 35 years have
narrow anterior chamber angles, but many never develop acute glaucoma.
Angle closure may be precipitated by pupillary dilation and thus can
occur from sitting in a darkened theater, at times of stress, or,
rarely, from pharmacologic mydriasis. Anticholinergic or
sympathomimetic agents (eg, nebulized bronchodilators, atropine for
preoperative medication, antidepressants, or nasal decongestants) are
also causes. Secondary acute angle-closure glaucoma may be observed
with anterior uveitis, dislocation of the lens, or topiramate therapy.
Symptoms are the same as in primary acute angle-closure glaucoma, but
differentiation is important because of differences in management.
Chronic angleclosure glaucoma is particularly common in eastern Asia.
It presents in the same way as open-angle glaucoma (see below).

Patients with acute glaucoma usually seek treatment
immediately because of extreme pain and blurred vision, though there
are subacute cases. The blurred vision is associated with halos around
lights. Nausea and abdominal pain may occur, and acute glaucoma must be
remembered in the differential diagnosis of the acute abdomen. The eye
is red, the cornea steamy, and the pupil moderately dilated and
nonreactive to light. Intraocular pressure is usually over 40 mm Hg.

Acute glaucoma must be differentiated from conjunctivitis, acute uveitis, and corneal disorders (Table 7-1).

Untreated acute angle-closure glaucoma results in severe
and permanent visual loss within 2–5 days after onset of symptoms.
Affected patients need to be kept under review for development of
chronic glaucoma.

Chronic glaucoma is characterized by gradually
progressive—over a period of months or years—excavation (“cupping”) and
pallor of the optic disk with loss of vision varying from slight
constriction of the peripheral fields to complete blindness. In chronic
openangle glaucoma, the intraocular pressure is elevated due to reduced
drainage of aqueous through the trabecular meshwork. In chronic
angle-closure glaucoma, flow of aqueous into the anterior chamber angle
is obstructed. In normal-tension glaucoma, intraocular pressure is not
elevated above the normal range but the same pattern of optic nerve
damage occurs, probably due to vascular insufficiency.

The cause of the reduced drainage of aqueous in primary
open-angle glaucoma has not been clearly established. A number of
mutations, such as in the myocilin gene on
chromosome 1, have been identified in a small proportion of cases. The
disease is bilateral, and there is an increased prevalence in
first-degree relatives of affected individuals and in diabetics. In
blacks, primary open-angle glaucoma is more frequent, occurs at an
earlier age, and results in more severe optic nerve damage. Secondary
open-angle glaucoma may result from uveitis or the effects of trauma.
Elevation of intraocular pressure is also a complication of steroid
therapy, whether it be topical, systemic, inhaled, or administered by
nasal spray.

In the United States, it is estimated that 2% of people
over 40 years of age have glaucoma, affecting more than 2 million
individuals and being three times more prevalent in blacks. At least
25% of cases are undetected. Over 90% of cases are of the open-angle
type, either primary open-angle or normal-tension glaucoma. Worldwide,
about 50% of all cases of glaucoma are due to acute (see above) or
chronic angle closure due to the very high prevalence of angle closure
in Asians.

Because patients with chronic glaucoma have no symptoms
initially, diagnosis is often made incidentally at routine eye tests.
On examination, there may be slight cupping of the optic disk observed
as an absolute increase—or an asymmetry between the two eyes—of the
ratio of the diameter of the optic cup to the diameter of the whole
optic disk (cup-disk ratio). (Cup-disk ratio of greater than 0.5 or
asymmetry of cup-disk ratio of 0.2 or more is suggestive.) Changes in
the retinal nerve fiber layer may be observed as an earlier finding in
some patients. The visual fields gradually constrict, but central
vision remains good until late in the disease.

Diagnosis requires consistent and reproducible
abnormalities in at least two out of three parameters— intraocular
pressure, optic disc cupping, and central visual field. The normal
range of intraocular pressure is 10–21 mm Hg. In many individuals,
elevated intraocular pressure is not associated with optic disk or

visual
field abnormalities. These ocular hypertensives are at increased risk
of developing glaucomatous damage. Treatment to reduce intraocular
pressure is justified if there is a moderate to high risk of the
development of glaucoma. Risk is determined by several factors,
including age, optic disk appearance, level of intraocular pressure,
and corneal thickness. Conversely, a significant proportion of patients
with glaucoma have normal intraocular pressure when it is first
measured, and only repeated measurements identify the abnormally high
pressure. Furthermore, in patients with normal-tension glaucoma, the
intraocular pressure is always within the normal range despite repeated
measurement. There are many other causes of optic disk abnormalities or
visual field changes that mimic glaucomatous damage, and visual field
testing may prove unreliable in some patients, particularly the
elderly. Taken together, these factors mean that the diagnosis of
glaucoma is not always straightforward, hampering the effectiveness of
screening programs.

All persons over age 40 years should have intraocular
pressure measurement and optic disc examination every 2–5 years. In
diabetics and in individuals with a family history of glaucoma, annual
examination is indicated.

The prostaglandin analogs (latanoprost 0.005%,
bimatoprost 0.03%, and travoprost 0.004% once daily at night; or
unoprostone isopropyl 0.15% twice daily) are commonly used as
first-line therapy because of their efficacy, the convenience of
once-daily administration, and their lack of systemic side effects. All
may produce conjunctival hyperemia, permanent darkening of the iris and
eyebrow color, and eyelash growth. Latanoprost has been associated with
reactivation of uveitis and macular edema. Topical β-adrenergic
blocking agents such as timolol 0.25% or 0.5%, carteolol 1%,
levobunolol 0.5%, and metipranolol 0.3% solutions twice daily or
timolol 0.5% gel once daily may be used alone or in combination with a
prostaglandin analog. They are contraindicated in patients with
reactive airway disease or heart failure. Betaxolol, 0.25% or 0.5%, a
β-receptor selective blocking agent, is theoretically safer in reactive
airway disease but less effective at reducing intraocular pressure.
Brimonidine 0.2%, a selective α₂-agonist, and dorzolamide 2%
or brinzolamide 1%, topical carbonic anhydrase inhibitors, also can be
used in addition to a prostaglandin analog or a β-blocker (twice daily)
or as initial therapy when prostaglandin analogs and β-blockers are
contraindicated (brimonidine twice daily, dorzolamide and brinzolamide
three times daily). Both are associated with allergic reactions. The
combination drops Xalacom (latanoprost 0.005% and timolol 0.5%) used
once daily in the morning and Cosopt (dorzolamide 2% and timolol 0.5%)
used twice daily improve compliance when multiple medications are
required.

Apraclonidine, 0.5–1%, another α₂-agonist,
can be used three times a day to postpone the need for surgery in
patients receiving maximal medical therapy, but long-term use is
limited by drug reactions. It is more commonly used to control acute
rises in intraocular pressure such as after laser therapy. Epinephrine,
0.5–1%, and the prodrug dipivefrin, 0.1%, are being used much less
frequently because of adverse effects on the outcome of subsequent
glaucoma surgery. Pilocarpine 1–4% (and sometimes higher concentrations
in patients with dark irides) four times a day is little used because
of the induced myopia in younger patients and the pupillary
constriction that compromises vision in patients with cataract. Oral
carbonic anhydrase inhibitors (eg, acetazolamide) may still be used on
a long-term basis if topical therapy is inadequate and surgical or
laser therapy is inappropriate.

Laser trabeculoplasty is used as an adjunct to topical
therapy to defer surgery and is also advocated as primary treatment.
Surgery is generally undertaken when intraocular pressure is
inadequately controlled by medical and laser therapy, but it may also
be used as primary treatment. Trabeculectomy remains the standard
procedure. Adjunctive treatment with subconjunctival fluorouracil or
mitomycin is used perior postoperatively in difficult cases.
Viscocanalostomy and deep sclerectomy with collagen implant—two
alternative procedures that avoid a full-thickness incision into the
eye—may be as effective as trabeculectomy but are more difficult to
perform.

In chronic angle-closure glaucoma, laser peripheral
iridotomy or surgical peripheral iridectomy may be helpful in the early
stages.

Untreated chronic glaucoma that begins at age 40–45
years will probably cause complete blindness by age 60–65. Early
diagnosis and treatment can preserve useful vision throughout life. In
primary open-angle glaucoma—and if treatment is required in ocular
hypertension—the aim is to reduce intraocular pressure to a level that
will adequately reduce progression of visual field loss. In eyes with
marked visual field or optic disk changes, intraocular pressure must be
reduced to less than 16 mm Hg. In normal-tension glaucoma with
progressive visual field loss, it is necessary to achieve even lower
intraocular pressure such that surgery is often required.

Anterior uveitis is characterized by inflammatory cells
and flare within the aqueous. In severe cases, there may be hypopyon
(layered collection of white cells) and fibrin within the anterior
chamber. Cells may also be seen on the corneal endothelium as keratic
precipitates (KPs). In granulomatous uveitis, these are large
“mutton-fat” KPs, and iris nodules may be seen. In nongranulomatous
uveitis, the KPs are smaller and iris nodules are not seen. The pupil
is usually small, and with the development of posterior synechiae
(adhesions between the iris and anterior lens capsule), it also becomes
irregular.

Nongranulomatous anterior uveitis tends to present
acutely with unilateral pain, redness, photophobia, and visual loss.
Granulomatous anterior uveitis is more indolent, causing blurred vision
in a mildly inflamed eye.

In posterior uveitis, there are cells in the vitreous.
Inflammatory lesions may be present in the retina or choroid. Fresh
lesions are yellow, with indistinct margins, whereas older lesions have
more definite margins and are commonly pigmented. Retinal vessel
sheathing may occur adjacent to such lesions or more diffusely. In
severe cases, vitreous opacity precludes visualization of retinal
details.

Posterior uveitis tends to present with gradual visual
loss in a relatively quiet eye. Bilateral involvement is common. Visual
loss may be due to vitreous haze and opacities, inflammatory lesions
involving the macula, macular edema, retinal vein occlusion, or,
rarely, associated optic neuropathy.

The systemic disorders associated with acute
nongranulomatous anterior uveitis are the HLA-B27related conditions
ankylosing spondylitis, reactive arthritis, psoriasis, ulcerative
colitis, and Crohn’s disease. Behçet’s syndrome produces both anterior
uveitis with recurrent hypopyon in 5% of patients and posterior uveitis
with retinal vein occlusions on occasion. Both herpes simplex and
herpes zoster infections may cause nongranulomatous anterior uveitis.

Diseases producing granulomatous anterior uveitis also
tend to be causes of posterior uveitis. These include sarcoidosis,
tuberculosis, syphilis, toxoplasmosis, Vogt-Koyanagi-Harada syndrome
(bilateral uveitis associated with alopecia, poliosis [depigmented
eyelashes, eyebrows, or hair], vitiligo, and hearing loss), and
sympathetic ophthalmia following penetrating ocular trauma. Syphilis
produces a characteristic “salt and pepper” fundus, often with
surprisingly little visual loss unless there is also primary syphilitic
optic atrophy. In congenital toxoplasmosis, there is usually evidence
of previous episodes of retinochoroiditis. The principal agents
responsible for ocular inflammation in AIDS are cytomegalovirus, herpes
simplex and herpes zoster viruses, mycobacteria, cryptococcus,
toxoplasma, and candida.

Autoimmune retinal vasculitis and pars planitis (intermediate uveitis) are idiopathic conditions that produce posterior uveitis.

Retinal detachment, intraocular tumors, and central nervous system lymphoma may all masquerade as uveitis.

Anterior uveitis will usually respond to topical
corticosteroids. Occasionally, periocular steroid injections or even
systemic steroids may be required. Dilation of the pupil is important
to relieve discomfort and prevent posterior synechiae.

Posterior uveitis more commonly requires systemic
corticosteroid therapy and occasionally systemic immunosuppression with
agents such as azathioprine or cyclosporine. Pupillary dilation is not
usually necessary.

If an infectious cause is identified, specific
antimicrobial therapy may be indicated. In general, the prognosis for
anterior uveitis, particularly the nongranulomatous type, is better
than that for posterior uveitis.

Cataract is a lens opacity. Cataracts are usually
bilateral. They may be congenital (owing to intrauterine infections
such as rubella and cytomegalovirus, or inborn errors of metabolism
such as galactosemia); traumatic; or secondary to systemic disease
(diabetes, myotonic dystrophy, atopic dermatitis), systemic or inhaled
corticosteroid treatment, or uveitis. Senile cataract is by far the
most common type; most persons over age 60 have some degree of lens
opacity. Cigarette smoking increases the risk of cataract formation.

Even in its early stages, a cataract can be seen through
a dilated pupil with an ophthalmoscope or slitlamp. As the cataract
matures, the retina will become increasingly more difficult to
visualize, until finally the fundus reflection is absent and the pupil
is white.

Functional visual impairment is the prime criterion for
surgery. The cataract is usually removed by one of the techniques in
which the delicate posterior lens capsule remains (extracapsular).
Laser treatment may be required subsequently if the posterior capsule
opacifies. Ultrasonic fragmentation (phacoemulsification) of the lens
nucleus allows cataract surgery to be performed through a small
incision without the need for sutures, thus reducing the postoperative
complication rate and accelerating visual rehabilitation.

It is routine practice to insert an intraocular lens at
the time of surgery. This dispenses with the need for heavy cataract
glasses or contact lenses. Multifocal and accommodative intraocular
lenses have been used with some success to reduce the need for both
distance and reading glasses.

If surgery is indicated, lens extraction improves visual
acuity in 95% of cases and can have a profound impact on quality of
life, although expectations must be realistic. The remainder either
have preexisting retinal damage or develop perioperative or
postoperative complications.

The primary event in rhegmatogenous retinal detachment
is the development of a retinal tear. This is usually spontaneous,
related to changes in the vitreous, but may be secondary to trauma.
Spontaneous detachment occurs most frequently in persons over 50 years
of age. Myopia and cataract extraction are the two most common
predisposing causes. Once there is a tear in the retina, fluid vitreous
is able to pass through the tear and lodge behind the sensory retina.
This, combined with vitreous traction and the pull of gravity, results
in progressive detachment. The superior temporal area is the most
common site of detachment. The area involved rapidly increases, causing
corresponding progressive visual loss. Central vision remains intact
until the macula becomes detached.

The basis of traction retinal detachment is the
development of preretinal fibrosis, such as in association with
proliferative retinopathy secondary to diabetic retinopathy or retinal
vein occlusion. Serous retinal detachment results from accumulation of
subretinal fluid, such as in exudative age-related macular degeneration
or secondary to choroidal tumors.

On ophthalmoscopic examination in rhegmatogenous retinal
detachment, the retina is seen hanging in the vitreous like a gray
cloud. One or more retinal tears will usually be found on further
examination. In traction retinal detachment, there is irregular retinal
elevation with fibrosis. With serous retinal detachment, the retina is
dome-shaped and the subretinal fluid may shift position with changes in
posture.

All cases of retinal detachment must be referred
immediately to an ophthalmologist. During transportation, the patient’s
head is positioned so that the detached portion of the retina will fall
back with the aid of gravity. Treatment of rhegmatogenous retinal
detachment is directed at closing the tears. A permanent adhesion
between the neurosensory retina, the retinal pigment epithelium, and
the choroid is produced in the region of the tears by applying
cryotherapy to the sclera or laser photocoagulation to the retina. To
achieve apposition of the neurosensory retina to the retinal pigment
epithelium while this adhesion is developing, indentation of the sclera
with a silicone sponge or buckle; subretinal fluid drainage via an
incision in the sclera; and injection of an expansile gas into the
vitreous cavity may be required. Certain types of uncomplicated retinal
detachment may be treated by pneumatic retinopexy, in which an
expansile gas is initially injected into the vitreous cavity followed
by positioning of the patient’s head to facilitate reattachment of the
retina. Once the retina is repositioned, the tear is sealed by laser
photocoagulation or cryotherapy. All the stages of pneumatic retinopexy
can be performed under local anesthesia as an office procedure. The
last stage is the same as is used to seal retinal tears without
associated detachment as prophylaxis against recurrence.

In complicated retinal detachments—particularly those in
which fibroproliferative tissue has developed on the surface of the
retina or within the vitreous cavity, ie, traction retinal
detachments—retinal reattachment can be accomplished only by removal of
the vitreous, direct manipulation of the retina, and internal tamponade
of the retina with air, expansile gases, or even silicone oil. (The
presence of an expansile gas within the eye is a contraindication to
air travel, mountaineering at high altitude, and nitrous oxide
anesthesia. Such gases persist in the globe for weeks after surgery.)
(See Chapter 38.) Treatment of serous retinal detachments is determined by the underlying cause.

About 80% of uncomplicated rhegmatogenous retinal
detachments can be cured with one operation; an additional 15% will
need repeated operations; and the remainder never reattach. The
prognosis is worse if the macula is detached or if the detachment is of
long duration. Without treatment, retinal detachment often becomes
total within 6 months. Spontaneous detachments are ultimately bilateral
in up to 25% of cases.

Diabetic retinopathy is the leading cause of new
blindness among adults in the United States aged 20–65 years. It is
broadly classified as nonproliferative or proliferative.

Nonproliferative retinopathy
shows dilation of veins, microaneurysms, retinal hemorrhages, retinal
edema, and hard exudates. A major subgroup includes those patients in
whom visual loss develops owing to edema, exudates, or ischemia at the
macula (diabetic maculopathy). This is the most common cause of legal
blindness in maturity-onset diabetes.

Proliferative retinopathy is
characterized by neovascularization, arising from either the optic disk
or the major vascular arcades. Vitreous hemorrhage is a common sequela.
Proliferation into the vitreous of blood vessels, with their associated
fibrous component, leads to tractional retinal detachment. Without
treatment, the visual prognosis with proliferative retinopathy is
generally much worse than that with nonproliferative retinopathy.
Severe proliferative retinopathy is often complicated by maculopathy.

Nonproliferative retinopathy is occasionally present at
the time of diagnosis in type 2 diabetes. Treatment includes optimizing
control of blood glucose, blood pressure, and serum lipids. Institution
of intensive insulin therapy can be associated with temporary
exacerbation of retinopathy, with multiple cotton-wool spots. Laser
photocoagulation is helpful in the treatment of focal macular edema but
may also be used when there is diffuse macular edema, which may also
respond to intravitreal injection of corticosteroid. The presence of
macular edema can be detected only by stereoscopic examination of the
retina or by fluorescein angiography. The level of visual acuity is a
poor guide to the presence of treatable maculopathy—hence the need for
regular ophthalmologic follow-up.

Proliferative retinopathy must be recognized early and
treated by panretinal laser photocoagulation to prevent blindness.
Neovascularization is all too often diagnosed only at the time of
vitreous hemorrhage. In some patients, a “preproliferative” retinopathy
may be identified. Whether panretinal laser photocoagulation should be
undertaken at this time can be determined by the degree of retinal
ischemia as assessed by fluorescein angiography.

Surgical treatment (vitrectomy) is used either to remove
vitreous hemorrhage and thus allow perioperative panretinal laser
photocoagulation for the underlying retinal neovascularization, to deal
with retinal detachments involving the macula, to manage rapidly
progressive proliferative disease, or to treat persistent macular edema.

Patients with diabetes should have yearly
ophthalmoscopic examination through dilated pupils. Examination by an
ophthalmologist is advisable in type 1 diabetes of more than 5 years’
duration; at the time of diagnosis in type 2 diabetes; in early
pregnancy, prior to conception in women contemplating pregnancy, and
every 4–8 weeks throughout pregnancy; if ocular symptoms develop; or if
there are suspicious findings of retinopathy, especially
neovascularization or macular exudates. Failure to diagnose diabetic
retinopathy by ophthalmoscopic examination is common, particularly if
the pupils are not dilated. The severity of diabetic retinopathy can be
decreased by control of blood glucose levels, but good diabetic control
is more important in preventing the development of retinopathy than in
influencing its subsequent course. Proliferative diabetic retinopathy,
especially after successful laser treatment, is not a contraindication
to treatment with thrombolytic agents, aspirin, or warfarin unless
there has been recent vitreous or preretinal hemorrhage.

Systemic hypertension affects both the retinal and
choroidal circulations. The clinical manifestations vary according to
the degree and rapidity of rise in blood pressure and the underlying
state of the ocular circulation. The most florid disease occurs in
young patients with abrupt elevations of blood pressure, such as may
occur in pheochromocytoma, malignant hypertension, or
preeclampsia-eclampsia.

Chronic hypertension accelerates the development of
atherosclerosis. The retinal arterioles become more tortuous and narrow
and develop abnormal light reflexes (“silver-wiring” and
“copper-wiring”). There is increased venous compression at the retinal
arteriovenous crossings (“arteriovenous nicking”), an important factor
predisposing to branch retinal vein occlusions. Flame-shaped
hemorrhages occur in the nerve fiber layer of the retina.

Acute elevations of blood pressure result in loss of
autoregulation in the retinal circulation, leading to the breakdown of
endothelial integrity and occlusion of precapillary arterioles and
capillaries. These pathologic changes are manifested as cotton-wool
spots, retinal hemorrhages, retinal edema, and retinal exudates, often
in a stellate appearance at the macula. In the choroid,
vasoconstriction and ischemia result in serous retinal detachments

and
retinal pigment epithelial infarcts. These infarcts later develop into
pigmented lesions that may be focal, linear, or wedge-shaped. The
abnormalities in the choroidal circulation may also affect the optic
nerve head, producing ischemic optic neuropathy with optic disk
swelling. Malignant hypertensive retinopathy was the term previously
used to describe the constellation of clinical signs resulting from the
combination of abnormalities in the retinal, choroidal, and optic disk
circulation. When there is such severe disease, there is likely to be
permanent retinal, choroidal, or optic nerve damage. Precipitous
reduction of blood pressure may exacerbate such damage.

In conditions characterized by thrombocytopenia or
severe anemia, various types of hemorrhages occur in both the retina
and choroid and may lead to visual loss. If macular hemorrhages have
not occurred, it is possible to regain normal vision with treatment.

Proliferative retinopathy (sickle cell retinopathy) is
particularly common in hemoglobin SC disease but may also occur with
other hemoglobin S variants. Severe visual loss is rare. Retinal
photocoagulation reduces the frequency of vitreous hemorrhage. Surgery
is occasionally needed for unresolving vitreous hemorrhage or
tractional retinal detachment.

If a patient complains of “something in my eye” and
gives a consistent history, a foreign body is usually present on the
cornea or under the upper lid even though it may not be visible. Visual
acuity should be tested before treatment is instituted, as a basis for
comparison in the event of complications.

After a local anesthetic (eg, proparacaine, 0.5%) is
instilled, the eye is examined with a hand flashlight, using oblique
illumination, and loupe. Corneal foreign bodies may be made more
apparent by the instillation of sterile fluorescein. They are then
removed with a sterile wet cotton-tipped applicator.
Polymyxin-bacitracin ophthalmic ointment should be instilled. It is not
necessary to patch the eye, but the patient must be examined 24 hours
later for secondary infection of the crater. If a corneal foreign body
cannot be removed in this manner, the patient should be referred to an
ophthalmologist.

Steel foreign bodies usually leave a diffuse rust ring.
This requires excision of the affected tissue and is best done under
local anesthesia using a slitlamp. Caution: Anesthetic drops should not be given to the patient for self-administration.

If there is no infection, a layer of corneal epithelial
cells will line the crater within 24 hours. The intact corneal
epithelium forms an effective barrier to infection, but once it is
disturbed the cornea becomes extremely susceptible to infection. Early
infection is manifested by a white necrotic area around the crater and
a small amount of gray exudate. These patients are referred immediately
to an ophthalmologist; untreated corneal infection may lead to loss of
the eye.

In the case of a foreign body under the upper lid, a
local anesthetic is instilled and the lid is everted by grasping the
lashes gently and exerting pressure on the mid portion of the outer
surface of the upper lid with an applicator. If a foreign body is
present, it can easily be removed by passing a wet sterile
cotton-tipped applicator across the conjunctival surface.

Intraocular foreign body requires emergency treatment by
an ophthalmologist. Patients giving a history of “something hitting the
eye”—particularly while hammering on metal or using grinding
equipment—must be assessed for this possibility, especially when no
corneal foreign body is seen, a corneal or scleral wound is apparent,
or there is marked visual loss or media opacity. Such patients must be
treated as for corneal laceration (see below) and referred without
delay. Intraocular foreign bodies significantly increase the risk of
intraocular infection.

A patient with a corneal abrasion complains of severe
pain and photophobia. There is often a history of trauma to the eye,
commonly involving a fingernail, piece of paper, or contact lens.
Visual acuity is recorded, and the cornea and conjunctiva are examined
with a light and loupe to rule out a foreign body. If an abrasion is
suspected but cannot be seen, sterile fluorescein is instilled into the
conjunctival sac: the area of corneal abrasion will stain a deeper
green than the surrounding cornea.

Treatment includes polymyxin-bacitracin ophthalmic
ointment, mydriatic (cyclopentolate 1%), and analgesics either topical
or oral nonsteroidal anti-inflammatory agents. Padding the eye is
probably not helpful. The patient should be reviewed within 48 hours to
be certain the cornea has healed. Recurrent corneal erosion may follow
corneal abrasions.

Contusion injuries of the eye and surrounding structures
may cause ecchymosis (“black eye”), subconjunctival hemorrhage, edema
or rupture of the cornea, hemorrhage into the anterior chamber
(hyphema), rupture of the root of the iris (iridodialysis), paralysis
of the pupillary sphincter, paralysis of the muscles of accommodation,
cataract, dislocation of the lens, vitreous hemorrhage, retinal
hemorrhage and edema (most common in the macular area), detachment of
the retina, rupture of the choroid, fracture of the orbital floor
(“blowout fracture”), or optic nerve injury. Many of these injuries are
immediately obvious; others may not become apparent for days or weeks.
Patients with moderate to severe contusions should be seen by an
ophthalmologist.

Any injury causing hyphema involves the danger of
secondary hemorrhage, which may cause intractable glaucoma with
permanent visual loss. The patient should be advised to rest until
complete resolution has occurred. Daily ophthalmologic assessment is
essential. Aspirin and any drugs inhibiting coagulation increase the
risk of secondary hemorrhage and are to be avoided. Sickle cell anemia
or trait adversely affects outcome.

Chemical burns are treated by irrigation of the eyes
with saline solution or plain water as soon as possible after exposure.
Neutralization of an acid with an alkali or vice versa generates heat
and may cause further damage. Alkali injuries are more serious and
require prolonged irrigation, since alkalies are not precipitated by
the proteins of the eye as are acids. It is important to remove any
retained particulate matter such as is typically present in injuries
involving cement and building plaster. This may require double eversion
of the upper lid. The pupil should be dilated with 1% cyclopentolate, 1
drop twice a day, to relieve discomfort and prophylactic topical
antibiotics should be started. In moderate to severe injuries,
intensive topical corticosteroids and topical and systemic vitamin C
are also necessary. Complications include mucus deficiency, scarring of
the cornea and conjunctiva, symblepharon (adhesions between the tarsal
and bulbar conjunctiva), tear duct obstruction, and secondary
infection. It can be difficult to assess severity of chemical burns
without slit-lamp examination.

Most ocular anti-infective drugs are administered
locally. Ointments have greater therapeutic effectiveness than
solutions, since contact can be maintained longer. However, they do
cause blurring of vision; if this must be avoided, solutions should be
used.

Systemic administration is required for all intraocular
infections, orbital cellulitis, dacryocystitis, gonococcal
keratoconjunctivitis, inclusion conjunctivitis, and severe external
infection that does not respond to local treatment.

The patient is placed in a chair with head tilted back,
both eyes open, and looking up. The lower lid is retracted slightly,
and 2 drops of liquid are instilled into the lower cul-de-sac. The
patient looks down while finger contact is maintained, so that the eyes
are not squeezed shut. Ointments are instilled in the same general
manner.

For self-medication, the same techniques are used except
that medications are usually better instilled with the patient lying
down.

Most eye bandages should be applied firmly enough to
hold the lid securely against the cornea. An ordinary patch consisting
of gauze-covered cotton is usually sufficient. Tape is applied from the
cheek to the forehead.

Eyelid taping, such as for corneal protection in facial
palsy, is best achieved with 1-inch-width transparent plastic adhesive
tape (eg, Transpore or even Sellotape) placed horizontally over the
closed eyelids from the side of the nose to the temple.

Unsupervised self-administration of local anesthetics is
dangerous because the patient may further injure an anesthetized eye
without knowing it. The drug may also interfere with the normal healing
process.

Dilating the pupil can very occasionally precipitate
acute glaucoma if the patient has a narrow anterior chamber angle and
should be undertaken with caution if the anterior chamber is obviously
shallow (readily determined by oblique illumination of the anterior
segment of the eye). A short-acting mydriatic such as tropicamide
should be used and the patient warned to report immediately if ocular
discomfort or redness develops. Angle closure is more likely to occur
if pilocarpine is used to overcome pupillary dilation than if the pupil
is allowed to constrict naturally.

Repeated use of local corticosteroids presents several
hazards: herpes simplex (dendritic) keratitis, fungal infection,
open-angle glaucoma, and cataract formation. Furthermore, perforation
of the cornea may occur when the corticosteroids are used for herpes
simplex keratitis. Topical nonsteroidal anti-inflammatory agents are
being used increasingly. The potential for causing or exacerbating
systemic hypertension, diabetes mellitus, gastritis, or osteoporosis
must always be borne in mind when systemic corticosteroids are
prescribed, such as for uveitis or giant cell arteritis.

Ophthalmic solutions are prepared with the same degree
of care as fluids intended for intravenous administration, but once
bottles are opened there is always a risk of contamination,
particularly with solutions of tetracaine, proparacaine, fluorescein,
and any preservative-free preparations. The most dangerous is
fluorescein, as this solution is frequently contaminated with P aeruginosa,
which can rapidly destroy the eye. Sterile fluorescein filter paper
strips are recommended for use in place of fluorescein solutions.

Whether in plastic or glass containers, eye solutions
should not remain in use for long periods after the bottle is opened.
Four weeks after opening is an absolute maximal time to use a solution
containing preservatives before discarding. Preservative-free
preparations should be kept refrigerated and discarded within 1 week
after opening.

If the eye has been injured accidentally or by surgical
trauma, it is of the greatest importance to use freshly opened bottles
of sterile medications or singleuse eyedropper units.

Patients receiving long-term topical therapy may develop
local toxic or hypersensitivity reactions to the active agent or
preservatives, especially if there is inadequate tear secretion.
Preservatives in contact lens cleaning solutions may produce similar
problems. Burning and soreness are exacerbated by drop instillation or
contact lens insertion; occasionally, fibrosis and scarring of the
conjunctiva and cornea may occur.

An antibiotic instilled into the eye can sensitize the
patient to that drug and cause an allergic reaction upon subsequent
systemic administration.

The systemic absorption of certain topical drugs (through the conjunctival vessels and lacrimal drainage

system) must be considered when there is a systemic medical
contraindication to the use of the drug. Ophthalmic solutions of the
nonselective β-blockers, eg, timolol, may worsen patients with
congestive heart failure or asthma. Atropine ointment should be
prescribed for children rather than the drops, since absorption of the
1% topical solution may be toxic. Phenylephrine eye drops may
precipitate hypertensive crises and angina. Also to be considered are
adverse interactions between systemically administered and ocular
drugs. Using only 1 or 2 drops at a time and a few minutes of
nasolacrimal occlusion or eyelid closure ensure maximum efficacy and
decrease systemic side effects of topical agents.