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196 CHAPTER 7: The Head and Neck
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in the primary position, the upper lid covers the limbus and a white scleral
strip usually shows between limbus and lower lid. Widening of the palpebral
ssure uncovers the upper border of the limbus exposing white sclera superiorly. When there is no actual proptosis, widened ssures produce the optical
illusion of global protrusion. A few normal persons have widened palpebral
ssures.
Exophthalmos, ocular proptosis. Proptosis is diagnosed by measurement.
If both eyes seem equally prominent, inspect them in prole (Fig. 7-29).
Unilateral proptosis is recognized by comparing the two eyes and suggests orbital tumor or inammation. Displacement medially suggests lacrimal gland disease, upwards suggests maxillary sinus disease, and laterally
implies ethmoid or sphenoid sinus disease. Graves disease is the most common cause of bilateral proptosis.
CLINICAL OCCURRENCE: Unilateral Exophthalmos: Graves disease, muco-
cele, orbital cellulitis and abscess, cavernous sinus thrombosis, orbital
periostitis, myxedema, orbital fracture, hemangioma, orbital neoplasm, arteriovenous aneurysm, fungal infection, histiocytosis; Bilateral Exophthalmos:
Graves disease, myxedema, acromegaly, cavernous sinus thrombosis, empyema of the sinuses, lymphoma, leukemia, histiocytosis.
Lid lag. Thyrotoxicosis increases sympathetic stimulation producing contrac-
tion of Mueller muscle in the upper lid. Lid lag indicates increased tone, even
without widened ssures in the primary position. It is usually bilateral and
occasionally one ssure is much wider than the other.
Other lid signs of hyperthyroidism.
bach Sign:
tion; Grifth Sign: Lower lids lag during globe elevation; Boston Sign: Jerking
of the lagging lid; Joffroy Sign: Absence of forehead wrinkling with upward
gaze, the head tilting down.
Narrowed palpebral ssures—enophthalmos. The globe is recessed in the
orbit. When bilateral, it is usually caused by decreased orbital fat or congenital microphthalmos. Unilateral enophthalmos results from trauma or inammation. The drooping eyelid in Horner syndrome produces an optical illusion
of globe recession.
Failure of lid closure—paralysis of orbicularis muscle. Damage to the
facial nerve (CN-VII) supplying the orbicularis oculi muscle, as in Bell
FIG. 7-29 Exophthalmos (Proptosis).
Tremor of the closed eyelids; Mean Sign: Globe lags during eleva-
Stellwag Sign: Infrequent blinking; Rosen-
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palsy, causes partial or complete orbicularis paralysis. When complete,
both upper and lower lids remain retracted, so the eye is unprotected, and
tears drain onto the face. Bell phenomenon is elevation of the globe while
attempting lid closure. Severe exophthalmos also prevents complete lid
closure.
Failure of lid opening—lid ptosis. Congenital ptosis is usually bilateral
from either paralysis of or failure to develop the levator palpebrae superioris. Acute acquired ptosis usually results from oculomotor nerve (CN-III)
In congenital ptosis there is lid lag as the child looks down. With
disease.
CN-III lesion, paralysis of other eye muscles may be present.
CLINICAL OCCURRENCE: Supranuclear lesions (e.g., encephalitis), Horner
syndrome, levator paralysis, levator dehiscence, thinning of levator tendon
(the lid droops but has normal excursion, 15–18 mm).
Blepharospasm. Unilateral or bilateral spasmodic lid closure, a focal dystonia, may interfere with function. Unilateral blepharospasm may follow Bell
palsy.
Epicanthal fold—Down syndrome. See page 242.
Shortened palpebral ssures—fetal alcohol syndrome. Shortened palpebral
ssures, epicanthic folds, shortened nose with anteverted nostrils, hypoplastic upper lip with thinned vermilion and attened or absent philtrum,
together with mental retardation, are stigmata of fetal alcohol syndrome.
Lid inversion—entropion. Structural changes or muscular contraction turns
the eyelashes inward to impinge upon the globe. Spastic entropion, caused by
increased orbicularis oculi tone, occurs only in the lower lids. The lid turns in
only when forcibly closed (Fig. 7-30A). Cicatricial entropion occurs in either
lid from contracture of scar tissue, as in trachoma. Irritation from the inverted
eyelashes may cause blepharospasm.
Lid eversion—ectropion. The lid turns outward (Fig. 7-30B). Both lids can
be affected by spastic or cicatricial ectropion, but paralytic ectropion only
involves the lower lid. Senile tissue atrophy sometimes results in ectropion
rather than entropion.
Violaceous lids. Heliotrope or violaceous discoloration of the periorbital skin
occurs in dermatomyositis.
FIG. 7-30 Pathologic Inversion and Eversion of the Eyelids.
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Lid erythema. Generalized reddening of the lids is nonspecic. Erythema of
the nasal half of the upper lid suggests frontal sinus inammation. Lacrimal
sac disease causes erythema of the medial lower lid. Hyperemia of the temporal upper lid suggests dacryoadenitis. The lid is frequently red over a sty.
Lid cyanosis. Blueness of the eyelid is caused by orbital vein thrombosis,
orbital tumors, and orbital arteriovenous malformations.
Lid hemorrhage. Blood extravasating into surrounding tissue after lid trauma
is colloquially known as a “black eye.” A palpebral hematoma results from a
nasal fracture. The appearance of hematoma many hours after head trauma
suggests a skull fracture; the greater the time interval, the more remote the
fracture site. Basal skull fractures produce a lid hematoma several days after
the event. Involvement of both eyes is raccoon sign.
Lid edema. Noninammatory edema is frequent in acute nephritis, but
uncommon in chronic nephritis and cardiac failure (Fig. 7-31A). Lid edema
is an early sign of myxedema and Graves ophthalmopathy. Lid edema is frequent in angioedema and trichinosis. Contact dermatitis frequently involves
the lids. The skin on the hands may not react to the allergen, but when transferred to the lids swelling occurs. Local infections cause inammatory lid
edema, readily identied by redness, warmth, and pain. Sagittal sinus and
cavernous sinus thrombosis are less common but serious causes of lid edema.
Xanthelasma. Xanthelasma are raised yellow, painless, and nonpruritic
plaques on the upper and lower lids near the inner canthi frequently associated with elevated cholesterol (Fig. 7-31B). They grow slowly and may disappear spontaneously.
Blepharitis. Seborrheic blepharitis is an oily inammation of the lid margins
producing greasy akes of dried secretion on the eyelashes and reddening
FIG. 7-31 Lesions of the External Eye. (See text for descriptions of each condition.)
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of the lid margins. Ulceration of the lid margin is usually staphylococcal
blepharitis. In angular blepharitis, caused by the diplococcus of Morax–Axenfeld
(Moraxella lacunata), the lid margins near the temporal canthi are inamed.
External hordeolum (sty). An eyelash follicle sebaceous gland is inamed
forming a pustule on the lid margin (Fig. 7-31C). It may be surrounded by
hyperemia and swelling. Many rupture and heal spontaneously.
Internal hordeolum and meibomian cyst (chalazion). An internal hordeolum or internal sty is acute inammation of a meibomian (tarsal) gland. A
chalazion or meibomian cyst is a granuloma of the gland (Fig. 7-31D). These
internal sebaceous gland lesions produce localized swelling frequently causing a protrusion on the lid. Everting the lid reveals hyperemia, a localized
cyst, or enlarged gland.
Dacryoadenitis. Lacrimal duct obstruction leads to acute lacrimal gland
inammation with pain and tenderness at the temporal edge of the orbit.
It must be distinguished from orbital cellulitis and upper lid hordeolum
(Fig. 7-31E).
Dacryocystitis. Nasolacrimal duct obstruction leads to inammation and
infection presenting as pain and overow of tears onto the cheek (epiphora).
Symptoms are increased by irritants such as wind, dust, or smoke. Tenderness,
swelling, and redness are present near the medial canthus beside the nose
(Fig. 7-31F). Swelling anterior to the eyelid distinguishes it from hordeolum.
Fluid can be expressed with pressure on the duct. Conjunctivitis, blepharitis,
and lid edema may be present.
Eye Movement Signs: Eye movement abnormalities are caused by either
primary extraocular muscle disease or disease of the central nervous system
and cranial nerves. Because distinguishing neurologic from primary muscle
disease is critical, these signs are discussed with the neurologic examination
in Chapter 14, Eye Movement Signs, page 657.
Restricted motion. Globe movement is restricted in all directions by tumors
in the orbit or increased orbital contents with Graves disease.
Glaucoma. See page 242.
Conjunctiva Signs
Subconjunctival vessels. The scleral vessels are prominent in some normal
individuals, running in from the sides (Fig. 7-32A).
Subconjunctival hemorrhage. Bleeding under the conjunctiva is obvious and
harmless (Fig. 7-32B). It can be induced by coughing, sneezing, weight lifting,
or defecation. Frequently, the cause is not apparent.
Conjunctival injection. Mild diffuse capillary hyperemia of the scleral
and palpebral conjunctivae, without hemorrhage, is common in the coryza
phase of respiratory infections and from exposure to direct sunlight or
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Red ciliary
PupilPupil
B. Iridic vesselsA. Conjunctival vessels
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FIG. 7-32 Vascular Disorders of the External Eye. A. Scleral vessels: These are the most prominent vessels
seen normally. B. Subconjunctival hemorrhage: Bright-red superficial blotches show through the sclera. They appear
suddenly and painlessly. C. Chemosis: The conjunctival edema may be demonstrated by pressing the lower lid against the
globe, producing a bulge in the boggy global conjunctiva above the point of compression.
flush
FIG. 7-33 Hyperemia and Congestion of the Globe. A. Hyperemic scleral vessels are superficial, coursing
radially from the periphery to the limbus in tortuous branches. B. Iritis: The vessels of the iris are deeper; when congested,
individual vessels are not visible, but they produce a pink or red band around the limbus, the ciliary flush.
environmental irritants. It may be mildly uncomfortable. Signicant pruritus,
pain, or discharge suggests another disorder, e.g., allergic conjunctivitis.
Conjunctival edema—chemosis. The conjunctiva is swollen and transparent, usually in association with lid edema. The edema is demonstrated by
inspecting the globe in prole while pressing the lower lid against the bulbar
conjunctiva; the lid edge pushes up a wave of edematous bulbar conjunctiva
(Fig. 7-32C). This is frequent in Graves ophthalmopathy.
Globe hyperemia and ciliary ush. Dilation of the radial conjunctival vessels
and their branches, running from the fornices toward the center of the cornea, causes bulbar conjunctival injection (Fig. 7-33A). Dilation of the deeper,
net-like episcleral vessels produces more violaceous injection, noted as ciliary
ush at the corneal limbus (Fig. 7-33B). Conjunctival suffusion blanches with
pressure; the ciliary ush does not blanch. Ciliary ush indicates uveal tract
inammation (see page 242).
Conjunctivitis. Inammation of the conjunctiva, regardless of cause, is conjunctivitis. The patient may awaken with eyelids stuck shut and a gritty or
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FIG. 7-34 Lesions of the Cornea and Iris. A. Pterygium: This abnormal growth of the pinguecula appears as a
raised, subconjunctival fatty structure, growing in a horizontal band toward a position over the pupil. B. Hypopyon: A collection of pus in the lowest part of the anterior chamber bet ween the cornea and the iris. C. Arcus senilis: A gray, opaque,
circular band in the cornea, separated from the limbus by a narrow, clear zone. D. Assessment of lacrimation: The
Schirmer test, see page 178. E. Staphyloma: Anterior protrusion of the cornea or sclera.
burning sensation with excessive lacrimation. There is marked hyperemia of
the palpebral and peripheral global conjunctival vessels in one or both eyes.
The many causes include viral and bacterial infections, foreign–body reaction, allergies, and blepharitis. DDX: Purulent discharge increases the probability for bacterial infection; itching suggests a nonbacterial etiology.
Hyperemic conjunctiva with calcification.
serum calcium–phosphorus product exceeds 70 in renal failure and sarcoidosis. Conjunctiva lesions: The segments from limbus to canthus at
7 to 10 o’clock and at 2 to 5 o’clock show hyperemic reddening, calcified
plaques, and pingueculae. The eyes are painful or feel gritty. The affected
areas contain calcium deposits, visible to the unaided eye or through the
slit lamp.
Cornea lesions: White material is visible in limbal arcs at 2 to
5 o’clock and 7 to 10 o’clock. This band keratopathy occurs with hypercalcemia and in renal disease with conjunctival calcification. The slit lamp
reveals calcium deposits.
Pterygium. Chronic irritation from wind and dust stimulates growth of the
pinguecula resulting in extension of a vascular membrane over the limbus
toward the center of the cornea. Usually bilateral, the resulting pterygium is
a raised, subconjunctival fatty structure, growing horizontally toward and
over the pupil (Fig. 7-34A), possibly obstructing vision. Its rm attachment
to the bulbar surface is strictly horizontal. A pseudopterygium is a band of scar
tissue extending in any direction and only partially adhering to the bulbar
conjunctiva, so a probe can pass beneath it.
Pigmented pingueculae. Brownish pigmentation of the pingueculae is a sign
of Gaucher disease. Others are hepatosplenomegaly, thrombocytopenic purpura, and patchy brown pigmentation on the face and the legs.
Lesions appear when the
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Cornea Signs
Hypopyon. Inammation in the iris or anterior chamber produces a purulent
discharge in the anterior chamber.
portion of the chamber is seen as a uid level behind the cornea (Fig. 7-34B).
Iritis is a common cause.
Lusterless cornea—supercial keratitis. Corneal inammation or drying
causes epithelial loss. The normal corneal luster is lost with graying of the
anterior stroma. A ciliary ush is often present. Fluorescein staining demonstrates ulceration or denuded epithelium. A corneal ulcer is extremely painful and causes miosis and photophobia. Disruption of the epithelium demands
urgent expert therapy, because visual loss can occur rapidly.
CLINICAL OCCURRENCE: Among the many causes of supercial keratitis
are contact lens-related ulcers, infected abrasions, herpes simplex and zoster,
corneal exposure, trigeminal nerve (CN-V) injury, amiodarone deposits, and
infection spreading from the conjunctiva.
Cloudy cornea—interstitial keratitis. Interstitial keratitis, deafness, and
notched teeth constitute the Hutchinson triad of congenital syphilis. Between
ages 5 and 15 years, faint central zone opacity is accompanied by a ciliary
ush, pain and lacrimation. Later, the cornea becomes diffusely clouded,
obscuring the iris. Blood vessels grow into the cornea. Corneal opacity is permanent. Acquired syphilis and tuberculosis are occasional causes.
Arcus senilis. A gray opaque band, 1.0–1.5-mm wide, is separated from the
limbus by a narrow clear zone (Fig. 7-34C). Initially, only a segment of the circumference is affected, later the circle is completed. It is present bilaterally in
many persons >60 years of age. If seen before age 40, suspect hyperlipidemia.
The opaque uid settling in the dependent
Keratoconjunctivitis sicca—Sjögren syndrome.
mal and salivary exocrine glands reducing tear ow leading to dry inamed
eyes. Sjögren syndrome is likely if persistent dry eyes, dry mouth, and a
positive Schirmer test (page 178 and Fig. 7-34D) are present without obvious
cause. HIV infection and sarcoidosis can produce similar ndings.
Kayser–Fleischer ring—Wilson disease. Copper deposited in the basement
membrane of the cornea’s endothelium is seen as a 2-mm-wide golden-brown
circular band in the peripheral cornea near the limbus. Beginning superiorly,
it spreads inferiorly. The neurologic manifestations of Wilson disease occur
simultaneously. A slit lamp is often required to see the ring.
Central corneal opacity. This results from trauma or infection and is seen in
75% of patients with Hurler syndrome.
Dots in the cornea—Fanconi syndrome. Cysteine crystals are deposited
throughout the stroma without an inammatory reaction.
Sclera Signs
Yellow sclera—icterus and fat. In obstructive jaundice (Chapter 9, page 414)
conjugated bilirubin colors the sclera evenly. The thicker conjunctiva in the
Lymphocytes inltrate lacri-
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fornices is usually deeper yellow. Fat deposits beneath the conjunctiva commonly impart a yellow color to the periphery, leaving the perilimbal area relatively white. This is more obvious with advancing age and anemia.
Red sclera—scleritis and episcleritis. Inammation of the sclera and/or
Tenon capsule reduces scleral integrity.
quently associated with autoimmune diseases. Patients have severe, deep,
boring pain. In sunlight, lesions appear red–purple. Suppurative scleritis is
rare and usually metastatic. Tuberculosis, sarcoidosis, and syphilis cause granulomatous scleritis with localized scleral elevation and nodules. Scleral thinning may be non-necrotizing or necrotizing (scleromalacia perforans) with acute
inammation surrounding an area of ischemia which may ulcerate. Episcleritis
is milder inammation involving the globe’s fascial sheath (Tenon capsule)
appearing clinically as diffuse or nodular violaceous injection (Fig. 7-35).
Blue sclera—osteogenesis imperfecta. Light reecting off the pigmented choroid
appears blue through the thinned sclera. This nding is classic for osteogenesis
imperfecta. It may be mimicked by minocycline deposits, scleral thinning after
scleritis, or age-related calcication of the horizontal rectus muscle insertions.
Brown sclera—melanin or homogentisic acid. Patches of melanin are commonly seen on the conjunctiva of dark-complexioned people, especially
blacks. In alkaptonuria with ochronosis, wedge-shaped areas of homogentisic acid, with their apices toward the limbus, color the sclera brown near the
ocular muscles attachments.
Scleral protrusion—staphyloma. Injury to the sclera and/or increased intraocular pressure lead to a protrusion from the surface of the globe. An anterior
staphyloma forming near the cornea creates a characteristic prole (Fig. 7-34E).
Pupil Signs: See Chapter 14, The Neurologic Examination, page 624.
Lens Signs
Cataract. Discoloration or disruption of the layers of the lens produces focal
or diffuse opacities that obstruct and/or scatter light before it reaches the retina. Because nearly all adults have some lens opacity, a clinical denition of
Scleritis, diffuse or nodular, is fre-
FIG. 7-35 Episcleritis. Because the episcleral vessels lie below the conjunctival vessels, the dilated episcleral arterioles
in episcleritis and uveitis has a violet hue.
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FIG. 7-36 Posterior Subcapsular Cataract. This cataract is just inside the posterior lens capsule. The melanosis of the
sclera is a normal variant in African Americans.
cataract implies interference with vision. Some cataracts are seen by shining a
light beam obliquely through the lens (focal illumination), by ophthalmoscopic
inspection against the red retinal reex with 0 diopter magnication from
~40 cm (15.7 inch), or by using + 10 diopter magnication with close inspection (direct illumination). Many are only identied by slit lamp. Centrally
placed cataracts are seen without pupillary dilatation; those in the periphery
are only visualized with dilation. This discussion is limited to cataracts detectable
without mydriatics or a slit lamp.
Anterior and posterior polar cataract. A small congenital white plaque is
seen in the center of the pupil resulting from a congenital defect in the anterior or posterior capsule.
Nuclear cataract. Yellow to brown discoloration, appearing rst in the central
lens, gradually becomes diffuse throughout the lens. A central black spot is
seen against the red retinal reex.
Cortical cataract. Wedge-shaped anterior or posterior cortical opacities,
arranged radially and extending in from the periphery, appear gray with the
penlight and black against the red retinal reex.
Secondary cataract. Posterior capsule brosis, a common sequela of cataract surgery, is more correctly an opacied posterior capsule, the lens being
absent. The peripheral lens epithelial cells migrate across the capsular bag left
to support the intraocular lens implant. It appears as dense tissue folds and
clusters of clear vesicles.
Diabetic cataract. Older diabetic patients have an increased tendency to
develop nuclear or cortical cataracts with no distinctive character. Juvenile
diabetic patients acquire distinctive snowake cataracts containing chalky
white deposits, the entire lens subsequently becoming milky.
Posterior subcapsular cataract. This lesion is commonly seen after longterm use of corticosteroids, with diabetes, and after trauma or uveitis
(Fig. 7-36).
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FIG. 7-37 Glaucoma: Optic Atrophy. The right eye of this darkly pigmented patient shows a deeply excavated cup
with a cup-to- disk ratio of 0.7–0.8. There is a large notch in inferior rim of the optic nerve, thinning of the rim elsewhere, and
a disc hemorrhage nasally all consistent with advanced glaucoma. The remaining rim is pink. The cribriform plate can be seen
in the base of the cup superiorly. Note the normal variation in the choroidal pattern of dark pigment and choroidal vessels.
FIG. 7-38 Displacement of the Lens. A. Subluxation. B. Anterior chamber dislocation.
Lens subluxation and dislocation. Rupture of the zonula ciliaris (zonule of
Zinn) permits the lens to move from its xed position behind the pupil. Slight
displacement, with the lens still backing the pupillary aperture, is subluxation
(Fig. 7-38A), manifested by tremulousness of the iris (iridodonesis) when the eye
moves horizontally. Viewed through the ophthalmoscope, the equator of the
lens may show as a dark, curved line crossing the pupil; a double image of the
retina with different magnications may be seen, one through the lens, the other
without the lens. A completely displaced lens is a dislocation. It is easily seen if
it enters the anterior chamber (Fig. 7-38B). Lens displacement is usually caused
by trauma. Nontraumatic dislocation occurs in several hereditary conditions
including Marfan disease, homocystinuria, and hereditary spherophakia.
Intraocular pressure changes. Increased tension occurs in glaucoma;
decreased tension is seen with myotonic dystrophy, globe rupture, and
extreme dehydration. Accurate pressures are obtained with a tonometer.
Retina Signs
Increased cup-to-disk ratio—glaucoma. See page 242 and Fig. 7-37.
Myelinated nerve bers. Optic nerve ber myelination usually ends at the
lamina cribrosa. Infrequently myelin sheaths continue into the retinal nerve
ber layer (Fig. 7-39B). Semi-opaque white patches emerging from the optic
disk spread into one or two retinal quadrants. The disk margin appears
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