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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3156_Библиотеки_им_академика_М_И_Перельмана.pdf
2. Ocular bobbing is characterized by fast, conjugate, downward movement of the eye,
followed by a slow drift to the primary position of gaze. This is seen in comatose patients
with large pontine lesions (e.g., hemorrhage, stroke, or tumor). Obstructive hydrocepha-
lus or metabolic encephalopathy can also cause this type of eye movement.
3. Superior oblique myokymia is characterized by small unilateral, vertical, and rotatory
movements of one eye. Symptoms of oscillopsia worsen when looking downward
and inward. This is usually benign and self-limited, but has been noted with multiple
sclerosis.
4. Essential head tremor. Nystagmus may occur with essential head tremor in which case
there is often a family history of same. The head tremor and related nystagmus may be
extinguished by fixing the head position or by utilizing a β-blocker.
B. Clinical Manifestations. The clinical manifestations of nystagmus were discussed in
Section II.A. Because many forms of nystagmus localize to the posterior fossa or are associ-
ated with a demyelinating disorder, an MRI is the imaging modality of choice if the cause is
otherwise not identified. In a patient with opsoclonus, an abdominal computed tomography
(CT) scan or an MRI should be done to look for a neuroblastoma involving the adrenal
glands. An abdominal ultrasound or CT scan is needed to evaluate the kidneys if aniridia
is present, as there is a significant incidence of associated Wilms’ tumor. As noted above,
neurology and ophthalmology consultation(s) should be requested as indicated.
REFERENCES
1. Leigh RJ, Zee DS. The neurology of eye movements, 4th ed. Oxford: Oxford University Press, 2006.
2. Straube A, Bronstein A, Straumann D. Nystagmus and oscillopsia. Eur J Neurol 2012;19:6–14, doi:
10.1111/j.1468-331.2011.03503.x
3. Serra A, Leigh RJ. Diagnostic value of nystagmus: spontaneous and induced ocular oscillations. J Neurol
Neurosurg Psychiatry 2002;73(6):615–618.
4. Simon JW, Kaw P. Commonly missed diagnoses in the childhood eye examination. Am Fam Physician
2001;64(4):623–628.
5. Swartz R, Longwell P. Treatment of vertigo. Am Fam Physician 2005;71(6):1115–1122.
6. Gottlob I. Nystagmus. Curr Opin Ophthalmol 2001;12(5):378–383.
5.6
I. BACKGROUND. Papilledema is an optic disc swelling produced by increased intracranial pres-
sure. It may be detected in the asymptomatic pediatric or adult patient during the course of
a screening funduscopic examination with a non–life-threatening cause. Conversely, it may
be identified in initially asymptomatic or gravely symptomatic patients (including pregnant
women) as a marker of a life-threatening condition such as subarachnoid hemorrhage, menin-
gitis, or brain tumor (1).
II. PATHOPHYSIOLOGY
A. Etiology.
True papilledema is always associated with increased intracranial pressure. The
differential diagnosis for papilledema includes trauma, primary or metastatic intracranial
tumor, aqueductal stenosis (as is seen in certain types of congenital hydrocephalus), pseu-
dotumor cerebri (idiopathic intracranial hypertension; frequently misdiagnosed as migraine
headache) (2), subdural hematoma, subarachnoid hemorrhage, arteriovenous malforma-
tions, brain abscess, meningitis, encephalitis, and sagittal sinus thrombosis.
B. Epidemiology. Most patients with papilledema are adults. Many of the causes of papill-
edema (e.g., subarachnoid hemorrhage and cancer) are more common with advancing age.
Papilledema
Peter R. Lewis
78
Pseudotumor cerebri is most commonly discovered in adolescent females and young
women. Individuals with immunosuppression (e.g., human immunodeficiency virus [HIV]/
acquired immunodeficiency syndrome, chemotherapy, chronic prednisone therapy) are at
heightened risk for central nervous system (CNS) infections (e.g., meningitis, encephalitis,
and brain abscess) that may be associated with papilledema.
III. EVALUATION. The history and physical examination are tailored to the age, setting, and urgen-
cy of the patient presentation. Patients with an acute and rapid increase in intracranial pressure
with associated papilledema may be moribund and comatose, requiring emergent and expedited
assessment and care. In less urgent situations, patients may present with nonspecific symptoms
(e.g., headache) (1) that prompt an investigation, initially on the basis of the history and physi-
cal examination, for associated intracranial pressure and its cause. Alternatively, the search for
clues to the presence and the cause of increased intracranial pressure only begins subsequent to
the discovery of papilledema during the course of a screening funduscopic examination.
A. History. In the symptomatic patient, headache, nausea, vomiting, diplopia, focal weak-
ness, fever, neck stiffness, photophobia, and/or fleeting loss of vision (obscurations)—
especially with the head in dependent positions—raise the clinician’s index of suspicion
for increased intracranial pressure. Parents of infants or children may report increased head
size or decreased alertness. After probing patient complaints and associated symptoms, the
clinician should determine the presence or risk factors for vascular disease (including prior
stroke), cancer, trauma, or immunosuppression. A thorough medication and drug use his-
tory should also be obtained. Prescription medications which may result in papilledema
include tetracycline, lithium, and corticosteroids. Toxins which may lead to papilledema
include methanol and ethylene glycol. A family history of conditions related to increased
intracranial pressure should be elicited.
B. Physical Examination
1. This commences with a general assessment of the patient and vital signs, including blood
pressure and visual acuity. Rarely is a decrease in visual acuity seen in association with
increased intracranial pressure; if present, it typically suggests other causes (e.g., vein
occlusion, anterior ischemic optic neuropathy, or optic neuritis).
2. Additional components of a detailed ophthalmologic examination, including fundu-
scopic assessment, should be performed. If present, sixth nerve palsies are evidenced by
limited lateral gaze and may be associated with horizontal diplopia, whereas third nerve
palsies demonstrate a limitation in medial gaze, elevation, and accompanying eyelid
depression. Regarding the funduscopic examination in the asymptomatic patient, it is
necessary to take care to first determine if there is true disc edema or only pseudopapill-
edema (this may well require consultation with an ophthalmologist). Pseudopapilledema
is optic nerve head elevation caused by hyaline deposition (“drusen”) within the optic
nerve head itself and is reported to be more common in Caucasians (3). There is no
associated increased intracranial pressure or CNS pathology. When true papilledema is
present, it is typically bilateral. There are optic disc findings common to early versus later
stages of papilledema as well as acute versus chronic papilledema. Disc edema produces
an obscuring of the blood vessels’ margins. Tiny splinter hemorrhages are seen in and
around the optic nerve. An absence of spontaneous venous pulsations (SVPs) may be
seen in conjunction with true papilledema due to increased intracranial pressure. If SVPs
are present, there is normal intracranial pressure. Prominent retinal hemorrhages suggest
malignant hypertension or central retinal vein occlusion.
3. A complete head and neck examination to check for neck stiffness, temporal artery ten-
derness, pain in and around the eyes, and sinus tenderness is also important. Thorough
vascular and neurologic examinations of the head and neck are to be included. Measure
head circumference in infants and young children; check for bulging or prematurely
closed fontanels in the former group.
C. Testing. If true papilledema is found, laboratory testing and clinical imaging should be
directed at determining the cause and the severity of the associated increased intracranial
pressure. In urgent clinical presentations, patients should be referred to the Emergency
Department of the nearest hospital. Suggested laboratory tests include sedimentation rate,
79
C-reactive protein, and white blood count if CNS infection is suspected. Serologies for
HIV, syphilis, and herpes should be obtained as indicated. A lumbar puncture for the mea-
surement of opening pressure and a cerebrospinal fluid (CSF) examination to evaluate for
evidence of meningitis, tumor, or hemorrhage should be performed only after ruling out a
compressive lesion with a computed tomography (CT) scan or magnetic resonance imaging
(MRI). If true papilledema is suspected by the primary care clinician and/or confirmed in
consultation with an ophthalmologist, then diagnostic imaging is mandatory. A CT scan
with and without contrast should be ordered. If the CT scan is inconclusive, an MRI will
be particularly helpful to evaluate for brain stem and cerebellar lesions, which can obstruct
CSF flow—thereby leading to papilledema—in children and adults. An MRI angiography
may be required to identify a related vascular abnormality such as an aneurysm. A consulting
ophthalmologist may perform fluorescein angiography to assist with diagnosis and subse-
quent management. A CT scan is the preferred technique to evaluate for acute intracranial
bleeding. Neurology and/or neurosurgical consultation(s) may also be indicated depending
on the cause of the patient’s papilledema. An ultrasound of the optic disc may be used if the
diagnosis of pseudopapilledema is uncertain.
D. Genetics. Many of the underlying conditions associated with papilledema have genetic
contributions.
IV. DIAGNOSIS
A. Differential Diagnosis.
Disc swelling without increased intracranial pressure may be
caused by the following conditions:
1. Optic Neuritis. An afferent pupillary defect exists along with decreased vision and pain
on extraocular movement. Color vision will be decreased in this normally unilateral
condition. It may be seen with multiple sclerosis.
2. Malignant Hypertension (of essential or secondary causes, including severe preeclamp-
sia). Blood pressure is markedly elevated and the patient is symptomatic. The eye
findings may include bilateral prominent disc edema, flame hemorrhages that extend
peripherally, and cotton wool spots.
3. Central Retinal Vein Occlusion. This is characterized by a unilateral disc swelling with
very prominent flame and blot hemorrhages, without increased systemic blood pressure.
4. Anterior Ischemic Optic Neuropathy. This may be due to arteritis (e.g., temporal/“giant
cell”) presenting with headache, stiff neck, temporal tenderness, jaw claudication, and
elevated sedimentation rate. If undetected and untreated, severe visual loss in one eye
followed by visual loss of the other eye may occur. When arteritis is absent, typically no
symptoms are present except decreased vision. Associated conditions include systemic
hypertension, diabetes mellitus, and collagen vascular disorders.
5. Infiltration of the Optic Nerve. Tuberculosis granuloma, leukemic infiltrate, sarcoid-
osis, and metastatic disease are more common examples of infiltrative processes that may
involve the optic nerve. The infiltration can be unilateral or bilateral and can lead to
rapid loss of vision.
6. Leber’s Hereditary Optic Neuropathy. This usually affects males in the second or third
decade and is characterized by unilateral progressive loss of vision with disc swelling.
7. Diabetic Papillitis. This represents an ischemic infarction to the optic nerve in
advanced diabetics. This is often bilateral and causes mild disc elevation.
B. Clinical Manifestations. Chronic papilledema can result in optic atrophy (with
decreased optic nerve swelling) and progressive visual loss (initially peripheral) that may
progress to frank blindness. Such patients should be followed with serial perimetry (visual
field testing) by an ophthalmologist.
REFERENCES
1. Clinch CR. Evaluation of acute headaches in adults. Am Fam Physician 2001;63(4):685–692.
2. Brazis PW, Lee AG. Elevated intracranial pressure and pseudotumor cerebri. Curr Opin Ophthalmol
1998;9(6):27–32.
3. Giovannini J, Chrousos G. Papilledema. Accessed at eMedicine www.emedicine.com/oph/topic187.htm,
on June 4, 2012.
80
5.7
I. BACKGROUND. Anisocoria is defined as an inequality of pupillary size (diameter).
II. PATHOPHYSIOLOGY
A. Etiology
1. The pupil is a hole or aperture in the iris that permits the passage of light through to
the retina. Two muscles within the iris control pupillary size. The sphincter pupillae is a
circular muscle that controls pupillary constriction, or miosis. The dilator pupillae is a
radial muscle that controls pupillary dilation, or mydriasis.
2. The pupillary constrictor is innervated by fibers from the parasympathetic autonomic
nervous system. These fibers originate in the midbrain and travel to the Edinger-
Westphal nucleus in the dorsal midbrain, and then with the third cranial nerve (CN III,
the oculomotor nerve) through the cavernous sinus to the orbit. They diverge from CN
III to synapse in the orbit with the ciliary ganglion. Postganglionic short ciliary nerves
then innervate the pupillary constrictor muscle. Lesions at any anatomic site along this
pathway lead to pathologic mydriasis (1).
3. The pupillary dilator muscle is innervated by fibers from the sympathetic autonomic
nervous system. These neurons originate in the hypothalamus, descend through the
brain stem to the C8-T2 lateral horn, and then travel with the cervical sympathetic
trunk to the superior cervical ganglion. Postganglionic long ciliary nerves travel with the
internal carotid artery until the superior orbital fissure, where they diverge and continue
to the dilator pupillae muscle. These fibers both stimulate the dilator pupillae and inhibit
the pupillary constrictor and ciliary muscles. They also innervate the levator palpebrae
muscle and therefore contribute to eyelid elevation. Lesions at any anatomic site along
this pathway lead to pathologic miosis (1).
B. Epidemiology. Physiologic anisocoria is common, affecting perhaps as many as 20% of
normal individuals. The difference in pupillary size is small, usually <1 mm (2).
III. EVALUATION
A. History.
In most patients, anisocoria is discovered incidentally; presenting symptoms are
relatively uncommon. It is necessary to inquire about ocular symptoms such as pain, red-
ness, tearing, or photophobia. Any past history of eye disease, injury, surgery, or medications
should be elicited.
B. Physical Examination. The pupils should be examined in both dim and bright lights,
assessing both direct and consensual pupillary light reflexes. An afferent pupillary defect
(Marcus Gunn pupil) permits a consensual light reflex, but no pupillary constriction or
paradoxical pupillary dilation to direct light. In an efferent pupillary defect, pupillary con-
striction to both direct and consensual light reflexes is absent.
1. The critical first step in assessing a patient with anisocoria is to determine which is the
abnormal pupil (i.e., Is one pupil abnormally constricted or is the other pupil abnor-
mally dilated?). It is necessary to examine the pupillary responses in both bright and dim
lighting. The pupil that does not dilate in dim light or constrict in bright light is the
abnormal one.
2. Extraocular movements should be tested. In patients with third nerve palsy, the affected
eye shows outward deviation during primary gaze. It is able to come to midline only with
attempts at inward gaze, and downward gaze leads to inward rotation.
C. Testing. Computed tomography or magnetic resonance imaging is valuable for suspected
intracranial mass lesions or bleeding. Angiography is indicated for suspected cerebral aneu-
rysm or carotid dissection. Consider obtaining chest radiography to evaluate for occult lung
Pupillary Inequality
David C. Holub
81
malignancy in patients with Horner’s syndrome (triad of miosis, ptosis, and unilateral facial
anhidrosis).
IV. DIAGNOSIS
A. Differential Diagnosis
1. The differential diagnosis of miosis includes Horner’s syndrome, unilateral anterior
uveitis, Lyme disease, or syphilis.
2. The differential diagnosis of mydriasis includes palsy of or damage to CN III, Adie’s
pupil, the use of certain medications (with anticholinergic effects), trauma, and acute
angle closure glaucoma.
B. Clinical Manifestations
1. Pathologic miosis may be caused by a lesion or disease state that affects any anatomic
site from the brain to the pupil itself. Horner’s syndrome is the triad of miosis with
ptosis and ipsilateral facial anhidrosis (variably present depending on the level of the
lesion). It is caused by damage to the cervical thoracic sympathetic fibers. A brain
stem stroke may lead to these findings. Disease of the internal carotid artery, such as
dissection, may also interrupt the signals normally carried by these nerves. Horner’s
syndrome also frequently occurs due to tumors that compress these nerve fibers. These
may include parotid gland tumors, carotid body tumors, lymphoma with enlarged cer-
vical adenopathy, mediastinal tumors, or apical lung tumors (typically in the superior
sulcus). Direct trauma can also damage the sympathetic nerve fibers (3). Miosis may
also be caused by unilateral ocular disease such as anterior uveitis, in which inflamma-
tion leads to the development of adhesions (synechiae) between the iris and the anterior
lens capsule. Lyme disease and neurosyphilis may involve the eye as well, leading to an
Argyll Robertson pupil—an irregular pupil that reacts poorly to light but normally to
accommodation.
2. Pathologic mydriasis is typically caused by disease states that affect the oculomotor
nerve (CN III) and thereby the parasympathetic fibers that travel with this nerve. Other
clinical manifestations of a third nerve palsy include abnormalities of ocular movement
and ptosis. Neurologic diseases such as multiple sclerosis may cause third nerve palsy.
Nerve compression can occur from vascular phenomena (posterior communicating
artery aneurysm), increased intracranial pressure due to head trauma with bleeding, or
an intracranial mass. In the comatose patient with head trauma, a temporal lobe hernia-
tion compressing the midbrain may also lead to unilateral mydriasis. Unilateral mydriasis
may also be an isolated finding in Adie’s pupil, caused by damage to the ciliary ganglion
through infection, ischemia, or trauma. Patients are typically women, 20–50 years of
age, and usually asymptomatic. They present with anisocoria, diminished or absent light
reflexes (both direct and consensual), and an exaggerated and prolonged (tonic) pupillary
constriction during accommodation.
3. Unilateral pharmacologic mydriasis may occur with anticholinergic medications.
4. Acute angle closure glaucoma is a crucial consideration in the evaluation of unilateral
mydriasis. Patients present with eye pain, redness, and visual impairment. An examina-
tion reveals a fixed, mid-dilated pupil and elevated intraocular pressure.
REFERENCES
1. Mosenthal W. A textbook of neuroanatomy. London: Parthenon Publishing, 1995.
2.
Eggenberger E. Anisocoria. Accessed at http://emedicine.medscape.com/article/1158571-overview on
May 2012.
3.
Bardorf C. Horner syndrome. Accessed at http://emedicine.medscape.com/article/1220091-overview on
May 2012.
82
5.8
I. BACKGROUND
A. The red eye is one of the most common ocular complaints encountered in primary
care. Although many causes of the red eye are benign, some are true emergencies.
Failure to act accordingly may pose an immediate threat to the patient’s vision.
B. Anatomically, almost any structure in the eye or its surrounding tissues may manifest
with redness.
II. PATHOPHYSIOLOGY
A. Etiology.
The primary causes of a red eye are infection or trauma to the various anatomic
structures of the eye. Occasionally, connective tissue disease or a primary ocular disease can
also manifest with a red eye. Causes include the following:
1. Scleritis is an inflammation of the sclera, the fibrous outer envelope of the eye.
2. Episcleritis is an inflammation of the connective tissue that lies between the sclera and
the conjunctiva.
3. Conjunctivitis is an inflammation of the conjunctiva, the mucous membranes that line
the anterior surface of the eye and the posterior surface of the eyelid.
4. Blepharitis is an inflammation of the eyelid, which may itself appear red and make the
eye appear red as well.
5. A hordeolum is a superficial inflammatory granuloma of the eyelid that develops acute-
ly from an obstruction of the ocular sebaceous glands (Zeiss or meibomian glands).
6. A chalazion manifests similarly, but is a deeper-seated granulomatous obstruction of
these glands.
7. Acute dacryocystitis results from an obstruction and secondary infection of the lacri-
mal system.
8. Iritis or anterior uveitis involves an inflammation of the anterior part of the eye (iris
and ciliary body).
9. Keratitis occurs when the cornea, the transparent outer covering of the anterior eye,
becomes inflamed, infected, or traumatically injured, resulting either in a corneal abra-
sion or a corneal foreign body.
10. Hyphema, or hemorrhage into the anterior chamber, which also results from trauma,
may manifest with visible redness if the amount of bleeding is significant. Even relative-
ly minor trauma may lead to a subconjunctival hemorrhage, evident as a prominent
red area in the normally white sclera.
11. Acute angle closure glaucoma leads to a rapid rise in intraocular pressure and may
manifest as redness along with ocular pain, visual loss, headache, and nausea.
12. Contact dermatitis, atopic dermatitis, preseptal (periorbital) cellulitis, or orbital
cellulitis cause the skin and soft tissues surrounding the eye or involving the eyelid to
become inflamed or infected.
B. Epidemiology. Conjunctivitis is the most common eye complaint in the United States,
accounting for 30% of all acute ocular complaints (1).
III. EVALUATION
A. History.
An assessment of the red eye begins with questions regarding its location (unilat-
eral, bilateral, or unilateral spreading to bilateral); onset (sudden or gradual); duration (acute,
subacute, or chronic); inciting factors (such as trauma); and associated signs and symptoms.
Ocular pain, swelling, photophobia, or disturbances in visual acuity are frequently signs of
a more emergent condition. Other associated symptoms may include crusting, discharge,
itching, burning, tearing, dry eyes, or a foreign body sensation. Systemic symptoms such as
Red Eye
David C. Holub
83
fever, headache, abdominal pain, nausea/vomiting, rhinorrhea, or cough should be elicited.
A past history of similar ocular complaints is important. The patient should be asked about
the use of contact lenses or eye drops. The past medical history may include certain systemic
diseases that produce ocular involvement, such as syphilis, inflammatory bowel disease, and
some collagen vascular diseases (sarcoidosis, ankylosing spondylitis, reactive arthritis, rheu-
matoid arthritis, and Sjögren’s syndrome). There may also be a history of allergic or atopic
disorders such as asthma, eczema, or allergic rhinitis.
B. Physical Examination
1. The physical examination of the eye should always begin with an assessment of visual
acuity with a wall-mounted or handheld Snellen’s eye chart. Visual acuity should always
be measured either with the patient’s corrective lenses or through pinhole testing. Visual
disturbances owing solely to refractive error improve with the use of lenses or pinhole
testing. Visual impairment due to organic eye disease does not.
2. Once this has been completed, a significant portion of the physical examination can then
be easily accomplished in the primary care office setting without specialized equipment.
A visual inspection of the eye and its surrounding soft tissues is essential to determine
where the redness is located anatomically (i.e., sclera, conjunctiva, anterior chamber, eye-
lid, or periorbital tissues). Other notable findings include the presence of any lid swelling
or crusting, purulent discharge, tearing, erythema or swelling of the periorbital tissues,
or proptosis. Vesicular skin lesions near the eye suggest a herpes infection, which can
have severe consequences on any infected structures within the eye. A palpation of the
globe and surrounding soft tissues for firmness or tenderness should then be performed.
A limitation of or pain with extraocular movements should be assessed. Eyelid eversion
should be carried out to look for retained foreign bodies. Finally, a pupillary examination
should be undertaken to assess size, shape, and reactivity.
3. Further examination of the eye requires both the appropriate equipment and the skill to
use this equipment and interpret the findings correctly. Although this is feasible in the
primary care setting, clinicians should obtain ophthalmologic consultation at this time if
needed.
4. A slit lamp examination should be performed to assess for abnormalities of the anterior
chamber, such as the presence of red or white blood cells or visible floating particulate
matter (flare). The slit lamp is a more precise method for measuring anterior chamber
depth than lateral visual inspection of the eye with a penlight. The cornea, with the
application of fluorescein staining and the cobalt blue light source on the slit lamp, can
be assessed for abrasion, ulceration, or a foreign body. Some patients may be unable to
tolerate this examination due to pain or photophobia. In this instance, a topical anes-
thetic may be applied to the eye.
5. The measurement of intraocular pressure is important in the evaluation for acute angle
closure glaucoma. This can be accomplished with a Schiötz tonometer or a handheld
electronic tonometer pen in the primary care setting. In the ophthalmologist’s office,
gonioscopy (a visual inspection of the angle between the iris and cornea) can also be
performed.
6. A funduscopic examination should be undertaken, ideally after pupillary dilatation has
been effected through the installation of a mydriatic solution. As pupillary dilatation can
precipitate an attack of acute angle closure, it is essential that this diagnosis be excluded
prior to attempting this. Under direct ophthalmoscopy, the cornea, lens, and vitreous
humor can be assessed for pathology.
C. Testing. Relatively few studies are useful in the differential diagnosis of the red eye.
Cultures of purulent discharge are occasionally helpful if bacterial conjunctivitis is sus-
pected. Blood cultures and a complete blood count with differential are prudent in cases of
suspected orbital cellulitis. Computed tomography or magnetic resonance imaging should
be considered if true orbital cellulitis is suspected (as opposed to preseptal cellulitis involv-
ing only the eyelids) to rule out serious complications including abscess or cavernous sinus
thrombosis. Workup for rheumatologic disease may be considered in patients with iritis,
episcleritis, or scleritis (2).
84
IV. DIAGNOSIS
A. Differential Diagnosis.
Given the potential severity of some of the causes of red eye, the
primary care physician’s first priority is to determine if immediate intervention or ophthal-
mologic referral is warranted. The most serious causes of the acute red eye that need to be
ruled out include acute angle closure glaucoma, hyphema, orbital cellulitis, acute keratitis,
corneal ulcer, scleritis, and iritis/uveitis. Less serious causes include conjunctivitis (other
than gonococcal), lid disorders, and subconjunctival hemorrhages.
B. Clinical Manifestations
1. Acute angle closure glaucoma presents with severe unilateral eye pain and blurry
vision, often accompanied by visual halos, headache, abdominal pain, and nausea
and vomiting. The physical examination reveals a shallow anterior chamber either by
penlight or slit lamp examination, partially dilated pupils that respond poorly to light,
a hazy cornea, firmness of globe on palpation, and elevated intraocular pressure on
tonometry (3).
2. Scleritis typically presents with pain, tearing, photophobia, and decreased visual acuity.
Visible swelling accompanies the redness. Discharge is typically absent. Fifty percent of
the cases are bilateral.
3. Iritis or uveitis usually presents as blurred vision, pain, and photophobia affecting a
single eye. Discharge is typically absent, although occasionally patients may have watery
discharge. Physical examination reveals a sluggishly reactive pupil with pain and pho-
tophobia on both direct and consensual pupillary testing. Slit lamp examination also
reveals proteinaceous or cellular matter in the anterior chamber (cell and flare).
4. Keratitis commonly presents with severe eye pain, photophobia, and blurry vision. A
slit lamp examination with fluorescein staining identifies any disruption in the corneal
epithelium. Owing to its serious nature, this must be regarded as a corneal infection until
proven otherwise.
5. Hyphema may be preceded by a history of ocular trauma. Vision is impaired only with
a large quantity of blood in the anterior chamber. Physical examination shows visible
blood on slit lamp examination, a dilated pupil, and elevated intraocular pressure.
6. Orbital or preseptal (periorbital) cellulitis presents with visible erythema, swelling,
warmth, and tenderness of the skin and soft tissues surrounding the eye. The eyelid is
typically involved. Orbital cellulitis, a more serious infection, may manifest with fever,
proptosis, and abnormalities of vision or pupillary response. Extraocular movements may
also be limited. These findings are absent in preseptal cellulitis.
7. Conjunctivitis is the most common cause of eye redness and may be bacterial, viral,
or allergic in etiology. Allergic conjunctivitis usually begins bilaterally, as opposed
to infectious conjunctivitis, which often begins unilaterally and is then spread to
the other eye due to manipulation by the patient. Itching and tearing are common.
A discharge is ubiquitous—clear or watery in allergic or viral etiologies but purulent in
bacterial cases. Allergic conjunctivitis may be accompanied by other allergic symptoms
or physical examination findings. Although cultures of purulent discharge are often
negative, it is difficult to clinically distinguish between viral and bacterial conjunctivitis.
Typically, either cultures or empiric treatment with topical antibiotics was warranted.
A 10- minute in-office immunoassay for adenovirus, the most common etiologic agent
of viral conjunctivitis, is now available. It has high sensitivity and specificity compared
with polymerase chain reaction (4). Notable exceptions to the typically benign course of
infectious conjunctivitis are cases of gonococcal and chlamydial conjunctivitis. A history
of exposure to genital secretions is critical, as the course of the illness and the treatment
differ significantly.
8. Episcleritis appears similar to simple conjunctivitis. The redness may be deeper and
more localized than seen in conjunctivitis. Discharge is typically absent (1).
9. Blepharitis presents as redness, crusting, and often as a swelling of the eyelid. It com-
monly occurs in combination with conjunctivitis, a hordeolum (with associated eyelid
tenderness and possibly a visible abscess), or a chalazion (without associated eyelid
tenderness or abscess).
85
10. Dacryocystitis presents with unilateral redness, swelling, and tenderness over the
lacrimal sac, which is located inferonasal to the eye along the side of the nose. This
condition is seen almost exclusively in children and in patients over the age of 40 years.
11. Corneal abrasions, ulcerations, and foreign bodies manifest with a foreign body
sensation, eye pain, photophobia, and tearing. An examination with a slit lamp under
fluorescein reveals dark green staining in areas where the corneal epithelium has been
disrupted. Lid eversion is essential to search for retained foreign bodies. Corneal infec-
tions must first be excluded.
12. Subconjunctival hemorrhage appears as a localized reddish discoloration of the sclera
due to minor trauma (including sneezing or coughing).
REFERENCES
1. Silverman MA. Conjunctivitis. Accessed at http://emedicine.medscape.com/article/797874-overview on
May 2012.
2. Farina GA. Red eye evaluation. Accessed at http://emedicine.medscape.com/article/1216540-overview
on May 2012.
3. Porter RS, ed. The Merck manual of diagnosis and therapy, 19th ed. West Point, PA: Merck & Co, 2011.
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5.9
I. BACKGROUND. A scotoma is a focal area of vision loss in the patient’s visual field. Patients
commonly refer to a scotoma as a “blind spot.” Scotomata may be further categorized in several
different ways.
A. A scotoma may be classified by its location in the visual field. A central scotoma occurs at
the point of fixation and causes significant and immediately noticeable visual impairment
to the patient. A paracentral scotoma occurs near the point of fixation and is also usually
noticeable to the patient. A peripheral scotoma occurs away from the point of fixation at
the edge of the visual field. Peripheral scotomata may be asymptomatic and only discovered
on visual field testing performed for a different reason.
B. A positive scotoma manifests as a black spot in the patient’s visual field. A negative scotoma
manifests as a blank spot in the patient’s visual field. Patients are nearly always aware of
positive scotomata, but negative scotomata may only be detected during an ophthalmologic
examination.
C. An absolute scotoma indicates a complete loss of visual perception, whereas a relative
scotoma involves diminished but not absent light perception in the affected area.
A color scotoma defines diminished or lost color vision only.
D. The term scintillating scotoma has come into common usage by both patients and clini-
cians, typically in the context of a migraine with aura. This is something of a misnomer,
because scintillations and scotomata are distinct visual phenomena. That they frequently
occur together in a migraine with aura has led to the origin of this term.
II. PATHOPHYSIOLOGY
A. Etiology.
Everyone has a physiologic scotoma at the optic disc, the site where the optic
nerve enters the retina. Diseases that affect the optic nerve may cause an enlargement of this
scotoma to the point that it interferes with visual acuity. This manifests as a central sco-
toma. Diseases that affect the macula may also present with central scotoma as a prominent
Scotoma
David C. Holub
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symptom. Peripheral scotomata result from disease processes that affect either the retina or
the optic nerve at any point along the visual pathways. Table 5.9.1 lists the common causes
of both central and peripheral scotomata.
B. Epidemiology. The incidence of scotoma varies depending upon the associated disease
state. The strongest association is with optic neuritis. Sixty percent of patients with scotoma
due to optic neuritis will eventually develop multiple sclerosis (1).
III. EVALUATION
A. History.
Patients with a central scotoma report a visual field defect as a primary complaint.
Elucidating the exact type of scotoma, as outlined in the definitions above, is important
in anatomically localizing the responsible lesion. A focused history should assess for other
visual disturbances such as diminished visual acuity, diminished color vision, or ocular pain.
Neurologic symptoms may be found in patients with multiple sclerosis. Systemic symptoms
TABLE 5.9.1 Causes of Central and Peripheral Scotomata
Cause Optic nerve/macula Retina
Ocular disease Primary open angle glaucoma Retinal detachment
Age-related macular degeneration
Neurologic disease Optic neuritis (secondary to multiple
sclerosis)
Optic neuritis (idiopathic)
Vascular disease Temporal arteritis Retinal vasculitis
Retinal artery occlusion
Retinal vein occlusion
Rheumatologic disease Sarcoidosis with ocular infiltration Diabetic retinopathy
Endocrine disease Thyroid ophthalmopathy Cytomegalovirus retinitis
Infectious disease Ocular syphilis
Malignancy Optic nerve glioma
Optic nerve sheath meningioma
Intracranial tumor with optic nerve
compression
Paraneoplastic syndromes
Nutritional deficiency Thiamine deficiency
Vitamin B12 deficiency
Folate deficiency
Toxin exposure Lead exposure Chloroquine toxicity
Methanol exposure
Ethylene glycol exposure
Ethambutol toxicity
Isoniazid toxicity
Digitalis toxicity
Amiodarone toxicity
Nutritional amblyopia (due to chronic
tobacco or alcohol use)
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