Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Eye Examination
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Eye Examination
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Miosis = constricted pupil(s); mydriasis = dilated pupil(s).
II. Assess pupil size, shape, reactivity, and accommodation (i.e., constriction when eyes cross nasally).
Anisocoria refers to pupils of different size. This is normal in a proportion of the population, and baseline
pupil size should be established before one looks for a cause. Causes include cranial nerve III palsy (as
from diabetes mellitus, multiple sclerosis), uncal herniation (patient comatose, other CNS signs and
symptoms), Horner's syndrome (interruption of sympathetic innervation of eye causing miosis, ptosis,
ipsilateral decreased sweating (anhidrosis); may be secondary to lung cancer, etc.), Adie's syndrome
(parasympathetic dysfunction at or distal to the ciliary ganglion from trauma, etc., leading to unilateral
dilated pupil), ocular trauma or inflammation, prescription or OTC eye drops, or Argyll-Robertson pupil
(pupils may be small, accommodating to near vision but not reacting to light or painful stimuli; seen with
neurosyphilis or Lyme disease). Common causes of weak reactivity include the problems aforementioned
plus optic nerve and retinal disease. A dilated pupil is not indicative of pending herniation unless the
patient is comatose.
A. Swinging flashlight test. Normal is constriction on direct light and constriction when the
contralateral eye is stimulated (consensual reflex). A consensual constriction of a pupil with
absent direct response indicates an afferent pupillary defect (that is visual loss at the eye with
preserved brain function allowing consensual reflex). May be caused by optic neuritis, ischemic
optic neuropathy, chiasmal tumors, retinal artery or vein occlusion, retinal detachment, acute angle-
closure glaucoma, etc.
III. Ocular Motility. Check six cardinal positions of gaze, corneal light reflection, and the cover test.
Common causes of motility and alignment abnormalities include congenital and childhood-onset
strabismus, cranial nerve palsies (e.g., from diabetes), orbital trauma, Graves' disease, myasthenia gravis,
stroke, or brain tumor.
IV. Fluorescein Staining. Moisten fluorescein paper and gently touch to inner surface of lower lid. Disrupted
corneal epithelium will fluoresce under Wood's lamp or cobalt blue slitlamp. However, this may miss up to
21% of defects. A dendritic defect will be highlighted in herpes simplex keratitis. Don't forget the
usefulness of the slit lamp, if available.
V. Always check visual acuity and evert upper and lower lids to look for foreign body.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Eye Examination
VI. Topical Anesthetic. Can be used to differentiate topical problems such as foreign body and corneal
abrasions from deeper problems such as iritis and glaucoma. If pain resolves with topical anesthetic, this
finding is suggestive of, but does not prove, a superficial cause.
VII. Some Useful Drugs.
A. Mydriasis. Cyclopentolate: maximal dilatation at 25 to 75 minutes, lasting 6 to 24 hours;
homatropine: maximal dilatation is rapid, must be used TID or QID to maintain mydriasis;
scopolamine: dilatation at about 1 hour, must be used TID to QID.
B. Miosis. Pilocarpine in 0.25%, 0.5%, and 1.0%. Generally needed only once per day. See section on
acute glaucoma for exception.
C. Anesthesia. Tetracaine 1%, proparacaine 0.5%. These cause corneal toxicity with repeated use--
NEVER prescribe for home use.
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Optic Nerve And Visual Pathway
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Optic Nerve And Visual Pathway
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Strabismus and Esotropia. Ocular misalignment, affecting 4% of children, causing amblyopia (a vision
loss that is uncorrectable by refractive lenses), reduced stereo vision, and a deformed appearance. It is
described according to the direction of the misalignment: esotropia refers to an inturning of the eye;
extropia, an outward turning of the eye; and hypertropia, an upturning of the eye. It may also be
categorized as paralytic or nonparalytic depending on whether the involved eye moves at all. Paralytic
strabismus is suggestive of the possibility of a brainstem lesion. Amblyopia secondary to strabismus is
correctable if treatment is begun by 3-4 years of age. Once 6 to 7 years is reached, vision loss is generally
permanent.
A. Predominant causes in adulthood include cranial-nerve palsies, ocular myopathies, and
myasthenia gravis. Consider MS, diabetes, etc.
B. To determine misalignment, look at the corneal light reflex when the patient looks in all
directions. The light should be reflected on the same portion of the cornea bilaterally (that is, light
reflects off center of cornea bilaterally when child looks forward). Alternatively, use the cover test.
Cover each eye in turn as child looks at an object about 20 feet away. When the eye is covered, the
uncovered eye should not move in a normal individual. In those with strabismus, the uncovered eye
will move to focus properly on the object being looked at.
C. The four common childhood forms are:
1. Strabismus of visual deprivation. Often develops when clear vision is interrupted in one or
both eyes. The most serious underlying causes are retinoblastoma and optic nerve or
chiasmal tumors. Any strabismus in which there is visual loss at the onset of strabismus
must be investigated immediately.
2. Pseudostrabismus. Eyes are functioning well, but infant appears to have strabismus because
of exaggerated nasal skin and lids.
3. Esotropia.
a. Infantile esotropia (also known as congenital esotropia) (nonparalytic) - 20%.
An idiopathic form that is present at birth or develops in the first months of life. If it
is intermittent, it should resolve by 6 months of age and does not need to be
investigated before this age. Generally no systemic findings. If it is constant, it should
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Optic Nerve And Visual Pathway
be investigated immediately, since it is suggestive of a paralytic cause. Treat by
patching the normal eye. Permanent visual loss may occur if not treated by 4 years of
age.
b. Accommodative esotropia: 45% to 50%. Occurs in children who have a hyperopic
refractive error and must therefore accommodate to see clearly. Begins as intermittent
and then becomes permanent as vision gets worse. As part of this accommodative
effort, convergence is triggered, and esotropia may develop. This usually first appears
between 6 months to 7 years of age (2 years average) but may appear as early as 2
month of age. Treat with the use of refractive lenses.
c. Nonaccommodative esotropia. Results as a defect of vision in one eye generally as
a result of unequal refractive errors. May also be attributable to cataract formation or
corneal scars.
4. Treatment may be surgical for muscle imbalance, use of refractive lenses, or patching the
normal eye to allow the affected eye to regain strength and vision.
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Orbit, Eyelids, And Lacrimal Apparatus
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Orbit, Eyelids, And Lacrimal Apparatus
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Orbital Cellulitis. Infection of tissues posterior to the orbital septum. Rarely seen, it is typically caused by
extension of sinusitis (usually maxillary and ethmoid) or periorbital cellulitis. It is more likely to be seen in
children than adults. Presentation includes dull aching periorbital pain, conjunctival injection, fever, URI
symptoms, violaceous swelling, and tenderness of upper and lower lids, impaired vision, and limited
ocular movement. CT or MRI is necessary for diagnosis and to rule out orbital subperiosteal abscess and
tumor. Complications include orbital abscess, cavernous sinus thrombosis, brain abscess, and meningitis.
S. aureus, Strep. spp., Enterobacteriaceae, and rarely H. influenzae are bacterial pathogens. Consider
viruses, fungi, and parasites in the immunocompromised. In diabetics, think of mucormycosis. Treatment
includes IV antibiotics (e.g., ampicillin/sulbactam ± vancomycin). Other options include second- or third-
generation cephalosporins (e.g., IV cefuroxime, cefoxitin, or cefotetan). Appropriate surgical consultation
is necessary.
II. Periorbital Cellulitis. Infection confined to structures anterior to orbital septum. The possibility of orbital
extension must always be considered. Vision is normal, and ocular movements are intact. Adults may be
managed as outpatients with penicillinase-resistant antibiotics (such as amoxicillin-clavulanate) and daily
examinations. Children should be hospitalized because of a strong association with bacteremia, septicemia,
and meningitis.
III. Dacryocystitis and Dacryostenosis. Inflammation of the lacrimal sac, which is usually unilateral and
secondary to nasolacrimal duct obstruction.
A. Congenital. Usually presents by 3 to 12 weeks of age and generally resolves by 6 months. It can be
treated by BID massaging of the lacrimal duct area, although this is of questionable efficacy.
Antibiotics are used if infection develops (see below). Occasionally requires surgical probing to
open the duct.
B. Infectious. Mucopurulent discharge, excessive tearing, erythema, and tender swelling of the medial
lower lid are seen. Culturing of the purulent material expressed from the lacrimal punctum should
be performed to aid in antibiotic choice. Usual organisms include S. pneumocystis, S. aureus, H.
influenzae, and S. pyogenes. Use oral first generation cephalosporin, erythromycin, or penicillinase-
resistant penicillin. Daily examinations are necessary because orbital cellulitis is a possible
complication. Adults may warrant referral for dacryocystorhinostomy. Surgery may be indicated if
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Orbit, Eyelids, And Lacrimal Apparatus
abscess develops.
IV. Hordeolum (acute infection of anterior lid margin usually related to staphylococci).
A. Acute external hordeolum (stye). A stye is an infection of Moll's glands along the lash line. Exam
reveals a tender focal mounding of one eyelid that develops over days, often with pustule
formation. Treatment includes warm compresses BID to QID as well as topical or oral antibiotics
depending on severity. Pulling the affected lash may promote drainage. Expect spontaneous
drainage within one week. Rarely, if the stye does not drain, I&D is required along with systemic
antibiotics. Frequently, can be done in the office with an 18-g needle once the abscess is "pointing."
B. Acute internal hordeolum (chalazion). A chalazion is a chronic granulomatous inflammation in
the meibomian gland. It can become secondarily infected resulting in an acute internal hordeolum.
Acute chalazion is treated with oral antibiotics and warm compresses. The chronic chalazion will
continue to grow, and excision or steroid injection is required for cosmetic reasons or when vision
is affected.
V. Blepharitis (eyelid inflammation caused by chemicals, seborrhea, rosacea, or staphylococci)
A. Anterior blepharitis. Chronic bilateral inflammation of the skin, cilium follicles, or accessory
glands of the eyelids. Recurrent conjunctivitis, burning, and itching of the eyelids are common
complaints. The lid margins are erythematous with dry crusted areas. Treatment involves removing
crusts and cleaning the lid margins with diluted baby shampoo daily. Antistaphylococcal antibiotic
ointment (i.e., bacitracin or erythromycin) should be applied to the lid margins BID to QID for two
weeks, then nightly.
B. Posterior blepharitis. Chronic bilateral inflammation of the eyelids caused by inflammation and
plugging of the meibomian glands. Individuals with rosacea or seborrheic dermatitis of the scalp
and face are especially vulnerable to this posterior form. Treatment involves warm compresses,
expression of the meibomian gland secretions, and long-term systemic antibiotic therapy
(tetracycline 0.5 to 1 g/day in four divided doses or doxycycline 50 to 100 mg once or twice daily.
This information is written primarily for providers.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Orbit, Eyelids, And Lacrimal Apparatus
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: The Red Eye
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: The Red Eye
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Conjunctivitis. Conjunctival erythema/injection caused by hyperemia of superficial vessels. Etiology
includes infection, allergies, chemicals, and tear deficiency. May be accompanied by itching, burning, or
foreign-body sensation. Often discharge or drainage is present, and crusting of the eyelids may occur while
sleeping. Vision is generally not affected. If particularly severe symptoms, consider gonococcal disease. If
seen in a neonate, Chlamydia may be the culprit (usually 3 weeks of age).
A. Viral. The so-called "pink eye." Usually adenoviruses. Acute redness, watery discharge with
foreign-body sensation and preauricular lymphadenopathy. Usually self-limited but may last up to 2
weeks.
1. Treatment. Antibiotics are not helpful and are not indicated. Boric acid washes, which can
be obtained over the counter, often provide excellent symptomatic relief. Patients should
throw away eyeliner, etc., which may be a reservoir for infection. OTC drops (e.g., artificial
tears, Oxymetazoline) may help as well. Oxymetazoline should not be used in children
because of risk of toxicity.
B. Bacterial. Acute redness with copious purulent discharge. Usually Staphylococci spp.,
Streptococcus pneumoniae, and Haemophilus spp. Treatment: Treat with topical agents for 2-3
days EXCEPT gonococcal and chlamydial. Examples include sulfacetamide sodium, erythromycin,
fluoroquinolone, bacitracin or gentamicin drops or ointment. Avoid a neomycin because of a higher
chance of hypersensitivity. If no corneal destruction, gonococcal is treated with 1g IM ceftriaxone.
Refer if any evidence of corneal ulceration is noted. Treat chlamydia with oral tetracycline,
doxycycline, or erythromycin for 2 weeks. May use topicals concomitantly with the latter two
organisms.
C. Allergic. Often a history of atopic problems--allergic rhinitis, asthma, and eczema. Watery, red,
itchy eyes, without purulent drainage, but can see stringy mucoid discharge. May also see
"chemosis," which is boggy edema of conjuctivae that gives the sclera a jelly-like appearance.
Usually seen in late childhood/early adulthood and may be seasonal or perennial.
1. Treatment. Systemic treatment with antihistamines will help and are indicated if the patient
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: The Red Eye
has other allergic symptoms. If symptoms are isolated to the eye or not responsive to oral
therapy, topical mast cell stabilizers (e.g., cromolyn, lodoxamide) are recommended for mild
to moderate cases. Topical antihistamines can be used (e.g., levocabastine), NSAIDs (e.g.,
ketorolac) may also be useful. Topical vasoconstrictor/antihistamine combinations (e.g.,
Vasocon-A or Naphcon-A) work well and are now OTC. However, they may cause rebound
hyperemia with prolonged use.
II. Iritis.
A. Symptoms. Photophobia and ciliary injection of straight deep vessels radiating from the limbus.
The pupil is small and poorly reactive because of inflammation and distant vision may be impaired.
On slitlamp examination, white precipitates can be visualized on the posterior surface of the cornea,
and inflammatory cells in the anterior chamber appear as "dust particles". Topical anesthetic will
not relieve pain.
B. Etiology. Most common etiology is posttraumatic, but history should include questions about the
presence of collagen vascular and autoimmune diseases. Diseases commonly associated with iritis
include ankylosing spondylitis, sarcoidosis, juvenile rheumatoid arthritis, lupus, Reiter's syndrome,
Wegener's granulomatosis, brucellosis, leptospirosis, and Behçet's syndrome, among others.
C. Treatment. Blocking pupillary sphincter and ciliary body action with a cycloplegic agent (such as
0.25% scopolamine, 2% homatropine, or 1% cyclopentolate) will reduce pain and photophobia.
Topical corticosteroids are indicated to suppress inflammation, but patients should be seen by an
ophthalmologist if this diagnosis is considered.
III. Acute Closed-Angle Glaucoma.
A. General. This is an ocular emergency requiring immediate diagnosis and treatment. Caused
by the closure of an already narrow anterior chamber angle. It is more common in Asians,
hypermetropia, and elderly (physiologically enlarged lens).
B. Symptoms. Expect greatly decreased visual acuity with peripheral-field losses, orbital pain,
headache, mid-dilated fixed pupil, diffuse conjunctival hyperemia, steamy cornea, and elevated
intraocular pressures. Precipitants include being in a dark room (dilates pupil), stress, and certain
drugs (e.g., sympathomimetics or anticholinergics). Acute glaucoma may present as abdominal
pain, nausea and vomiting, and this diagnosis should not be overlooked in those with a GI
presentation. An ophthalmologist should be consulted immediately upon making the diagnosis.
C. Diagnosis. Is clinical along with the demonstration of an elevated intraocular pressure.
D. Treatment. Treat with acetazolamide 500 mg PO or IV followed by 250 mg Q6h with or without
topical beta-adrenergic antagonists (timolol maleate 0.5% one dose) to decrease aqueous humor
production. Constrict pupil with topical pilocarpine 2% one drop every 5 minutes for the first 2
hours. Vitreous humor volume can be decreased with systemic hyperosmotic agents such as
mannitol 1 g/kg IV. Sedate the patient, provide adequate analgesia, and refer immediately to an
ophthalmologist. Definitive treatment involves laser iridotomy or peripheral iridectomy.
IV. Corneal Abrasion.
A. General. A localized loss of epithelium from the cornea typically caused by foreign bodies,
fingernails, or contact lenses (i.e., direct trauma).
B. Symptoms. Sudden pain and foreign-body sensation in the eye; this is relieved by topical
anesthetics. There may be associated injection of the conjunctival vessels, tearing, and photophobia.
C. Diagnosis. Made by fluorescein staining. Carefully search for any remaining foreign bodies using
the slitlamp and everting the lids. Foreign bodies can be removed using a Q-tip or needle. Always
evaluate for a rust ring when the foreign body is metallic.
D. Treatment. Most heal in 24-48 hours. Topical antibiotics may reduce the risk of infection.
However, aminoglycosides may reduce the rate of reepithelialization. Avoid prescribing topical
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: The Red Eye
anesthetics as they retard healing and may lead to corneal epithelial breakdown. Topical steroids
also retard healing and increase infection risk. Tetanus status should be ascertained and updated, if
needed. Patching abrasions not related to contact lens use is traditional. However, recent evidence
indicates that patching may increase discomfort and decrease rate of healing. Patients should be
advised to avoid reading, watching TV, and other "eye-intensive" activities. Short-acting
cycloplegic agents (e.g., 0.25% scopolamine, 2% homatropine, or 1% cyclopentolate) decrease
severe pain by helping to reduce ciliary spasm. Close, daily follow-up care is required.
E. Contact lens-related and "dirty" abrasions (as from dogs, contaminated foreign body) should
never be patched and should be treated with an aminoglycoside antibiotic because of
increased risk of Pseudomonas infection. Patients with corneal ulcers should have an
ophthalmologic consultation.
V. Subconjunctival Hemorrhage. Sharply demarcated area of injection resulting from the rupture of small
subconjunctival vessels. Hemorrhages can result from trauma, bleeding diathesis, coughing, vomiting,
straining, or viral hemorrhagic conjunctivitis (adenovirus, enterovirus, and coxsackievirus). Excessive
rubbing from dry eyes may contribute. Sub-conjunctival hemorrhage alone is self-limited and requires no
treatment. The presence of blood in the anterior chamber indicates a hyphema and requires
immediate ophthalmologic referral.
VI. Hyperthyroidism May Cause Conjunctival Injection.
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Trauma
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Trauma
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Blunt Trauma.
A. Orbital wall fracture should be considered after any blunt eye trauma. Signs and symptoms may
include diplopia, epistaxis, ecchymosis, crepitus, hypesthesia in the infraorbital nerve distribution,
and restricted upward gaze secondary to inferior rectus entrapment. A CT scan with axial and
coronal cuts is necessary for definitive diagnosis. Plain facial films are frequently inadequate
although fluid in the sinus or fat protruding from the orbital floor are presumptive evidence of a
fracture. Visual impairment or globe injury warrants immediate referral.
B. Hyphema is the presence of blood in the anterior chamber and is typically easily visualized.
Symptoms include pain, photophobia, and blurring of vision. Elevated intraocular pressure is a
possible side effect and should be treated like acute angle closure glaucoma. Bed rest with elevation
of the head and patching of the affected eye may prevent the frequent complication of rebleeding,
but the data are unclear. Immediate ophthalmologic consultation should be obtained to determine
need for surgical evacuation.
C. Periorbital contusions are treated with ice, head elevation, and reassurance that symptoms will
resolve in 2 to 3 weeks.
D. Air Bag Trauma. Most common injuries are to the eyelids, conjunctiva, and cornea. Hyphemas
frequently occur. Less commonly seen are retinal detachment, scleral rupture, and lens dislocation.
Injuries are bilateral in 27%. All patients should get complete ophthalmologic exam because of this
high-velocity trauma. Can also get alkaline chemical keratitis from the NaOH produced during the
chemical reaction that inflates the bag.
II. Penetrating Trauma.
A. Corneal laceration, scleral laceration, intraocular foreign body, or globe rupture. Treatment
includes placement of a shield (an inverted paper or Styrofoam cup will do) without applying
pressure to the globe, initiation of systemic antibiotics to cover both gram-positive and gram-
negative organisms (such as vancomycin and gentamicin), tetanus prophylaxis, sedation, analgesia,
and urgent referral.
B. Chemical exposure (especially alkali). Expect to find lacrimation, bleph-arospasm, painful red
sclera, and photophobia. Direct lavage should be done at the scene for at least 15 minutes with any
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Trauma
water or saline solution available. To irrigate in the emergency department, instill a topical
anesthetic (Pontocaine, tetracaine and others). Sweep under lids and in conjunctival cul-de-sacs to
remove particulate matter. Hang IV solution bags of normal saline connected through IV tubing to
an l8-gauge plastic IV catheter or a continuous-flow contact lens. For patients who cannot tolerate
saline, balanced salt solution is a good, although expensive, alternative. Lavage should be
continued for at least 20 minutes by the clock. When adequately lavaged use litmus paper to
ensure that eye pH is neutral immediately after the lavage is completed and again 10 minutes later.
This is especially crucial to document in alkali injuries. Continue to irrigate until the pH is neutral
(pH 5 7.4 to 7.6). Once pH is normal, use fluorescein stain to evaluate for damage or residual
abrasions. Reapply ophthalmic anesthetic and apply two drops of 0.25% scopolamine, 2%
homatropine, or 1% cyclopentolate for cycloplegia into the affected eye or eyes if indicated by
severity of injury. This will prevent spasm of the pupil, which can cause pain. Use an antibiotic
ointment. Erythromycin is a good choice. Gentamicin and other aminoglycosides inhibit corneal
repair. Provide adequate oral analgesia and follow-up within 24 hours. Contact lenses should not be
worn for 2 weeks. Refer immediately for any of the following: (1) acid or alkali burn of
significance (that is, corneal epithelial damage, any haziness of cornea), or (2) subnormal visual
acuity, severe conjunctival swelling. See all others back in 24 hours. Prescribe oral pain
medications, since these are often painful injuries.
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Retina
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Retina
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Retinal Detachment. The separation of the neurosensory retinal layer from its underlying pigmented
epithelium. Patients will experience some degree of visual loss and may complain of cloudy vision,
floaters, flashes of light, or a black curtain across their vision. Risk factors include aging, myopia, eye
surgery, inflammation, trauma, a prior retinal detachment, or a family history of retinal detachment.
Funduscopic exam reveals a gray or opaque retina instead of the normal pink color. The arterioles and
venules may appear dark, and floaters may be visualized. Retinal detachment is an ocular emergency, and
prompt surgical intervention is necessary.
II. Retinal Vascular Occlusion. May involve either retinal arterial occlusions (resulting from embolism or
thrombosis), or venous occlusions (resulting from thrombosis). Both present as painless monocular vision
loss, with arterial occlusion occurring suddenly and venous occlusion causing vision to decrease over
hours. The patient may experience transient episodes of blindness before the final event.
III. Retinal Arterial Occlusion. On ophthalmoscopic exam, a small occlusion produces a flame-shaped
hemorrhage or a cotton-wool spot; a large occlusion produces a pale retina and a "cherry red spot" in the
area of the macula. Intermittent digital pressure should be applied to the globe in an attempt to dislodge the
embolus. Increasing the pCO2 to dilate the artery can be attempted if one has the patient breathe into a
paper bag or inhale carbogen. Urgent consultation should be obtained.
IV. Retinal Vein Occlusion. Ophthalmoscopic exam reveals a "blood-and-thunder optic fundus" - massive
hemorrhage covering the retinal surface and dilated veins. There is no immediate treatment for retinal vein
occlusion, and the deficits are often reversible. Look for a cause including hyperviscosity, hypertension,
glaucoma, and diabetes. These patients need to be followed by an ophthalmologist, since many will
develop neovascularization of the iris or retina.
V. Diabetic Retinopathy. Most common cause of blindness in middle adulthood. Prevalence increases with
duration of diabetes. Symptoms include blurred vision, floaters, field loss, and poor night vision. Non-
proliferative includes microaneurysms, hemorrhages, cotton-wool spots, lipid exudate, and macular
edema. Proliferative refers to neovascularization from optic disc, retina, or iris secondary to retinal
ischemia. These new vessels require laser photocoagulation. Tight glucose control reduces the
development and progression of this problem. Early detection/treatment are best to reduce vision loss: all
diabetics should see an ophthalmologist at least annually and at the time of initial diagnosis.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Retina
VI. Age-Related Macular Degeneration (ARMD). Most common cause of vision loss over age 65.
Prevalence increases with age: 11% ages 65-74 and 28% age over 75. Macula serves central vision but
symptoms can include blurred vision, image distortion (metamorphopsia), central scotoma, and trouble
reading. Risk factors: age, family history, cardiovascular disease, smoking, UV light, blue eyes, and
antioxidant vitamin deficiency. Two types exist: nonexudative or "dry" and exudative or "wet". 90% have
the dry form but this accounts for only 10-20% of severe vision loss. Dry is characterized by drusen
(deposits of extracellular debris that appear yellow on exam) and geographic atrophy (patches of dead
retinal layers). Wet is characterized by choroidal neovascularization secondary to retinal injury. These
vessels leak fluid and blood. Fibrosis develops months to years later leaving a macular scar. Laser
photocoagulation in can reduce severe vision loss in wet ARMD but only 10-13% of patients are
candidates. Recurrence is high and laser can worsen vision. Low vision aids help. Verteporfin, a light
activated drug which is administered IV, concentrates in new vessels sclerosing them. Experimental
treatments include: surgery, radiation, and antiangiogenic drugs (e.g., interferon alpha-2a and thalidomide).
Antioxidant supplements may help prevent ARMD but are controversial. Patients above age 65 should see
an eye doctor annually and use an Amsler grid periodically to self check for vision problems.
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
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Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Cornea And Lens
University of Iowa Family Practice Handbook, Fourth Edition, Chapter 19
Ophthalmology: Cornea And Lens
Matthew L. Lanternier, MD
Department of Family Medicine
University of Iowa College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby
I. Corneal Ulcers. The result of an epithelial defect with stromal infiltration. Ulcers of the cornea appear as
whitish, infiltrated areas surrounding a corneal epithelial defect. It is usually a complication of
conjunctivitis, contact lens use, or of a corneal abrasion. Soft contact and extended-wear lenses are up to
19 times more likely than daily-wear lenses to cause ulceration. Fluorescein examination will reveal the
lesion. Apply topical gentamicin or tobramycin hourly and obtain immediate ophthalmology consultation.
II. Optic Photalgia (Flash Burns, "Welder's Burns"). Occurs as a result of exposure to ultraviolet radiation
(welders, sun exposure, snow blindness) and generally presents several hours after the insult. Fluorecin
will show a epithelial keratitis with diffuse uptake in the cornea. Patch both eyes, bed rest, strong oral
analgesia, and sedation if necessary. If no reduction of symptoms is noted after 24 hours, refer. Topical
analgesics produce slow healing and may lead to additional injury.
III. Corneal Abrasions. See section on Red Eye.
IV. Corneal Transplantation. Successful procedure for restoring sight in corneal disease. Most common
indication is edema after cataract extraction. Rejection is a life-long risk and topical steroids are used to
reduce risk.
V. Cataracts. Most common cause of blindness worldwide. Common cause of vision loss in elderly. Can be
congenital but most are acquired. Some medications (e.g., steroids, including inhaled) and systemic
diseases (e.g., diabetes) can contribute. Prevalence increases with age: <5% prior to age 65 to up to 50%
>75 years old. UV light may accelerate progression but generally progress over months to years.
Symptoms include blurred vision, glare, and monocular diplopia. Treatment is surgical and done only
when vision loss interferes with everyday life. Most common technique is phacoemulsification (ultrasound
fragmentation of lens with aspiration). Artificial lens implants are placed. Posterior lens capsule
opacification occurs in up to 50% within 3-5 years. Treat with laser capsulotomy. Overall, >90% derive
visual improvement with surgery. Potential complications include glaucoma, vitreous loss, retinal
detachment and loss of vision, but complications occur in less than 1%.
file:///D|/MED/ophthalmology/Cornea%20And%20Lens.html (1 of 2)10/1/1994 7:59:52 PM
Virtual Hospital: University of Iowa Family Practice Handbook, Fourth Edition: Ophthalmology: Cornea And Lens
This information is written primarily for providers.
All contents copyright © 1992-2004 the Author(s) and The University of Iowa. All rights reserved.
file:///D|/MED/ophthalmology/Cornea%20And%20Lens.html (2 of 2)10/1/1994 7:59:52 PM
Handbook of Ocular Disease Management - Blepharitis
Blepharitis
SIGNS AND SYMPTOMS
Blepharitis is a generic term for several types of eyelid inflammation
usually surrounding the lid margin and eyelashes, including both
infectious and non-infectious forms. Chronic blepharitis is often linked
to an occupation that causes dirty hands, or poor hygiene in general.
The presentation is typically bilateral. Symptoms vary but may include
any or all of the following: itching, burning, scratchiness, foreign body
sensation, excessive tearing and crusty debris around the eyelashes,
especially upon waking. Visible ocular signs include lid erythema, collarettes (a fibrin crust encircling an
eyelash), madarosis (missing lashes), trichiasis (an inturned lash), plugged meibomian glands, conjunctival
injection and superficial punctate keratitis on the lower third of the cornea. There is often an associated
conjunctivitis with papillary hypertrophy of the palpebral conjunctiva.
PATHOPHYSIOLOGY
Though many types of lid inflammation exist, only those that affect lipid secretions are considered blepharitis.
The cause is either meibomianitis, seborrhea (excess sebum production), Staphylococcal infection, or some
combination of the three.
Excess lipid production by the meibomian glands is the most common form of seborrheic blepharitis, but the
condition can also occur from overactive sebaceous glands of the scalp, eyebrows and face as well. The
meibomian glands themselves are often inflamed, but not necessarily in all cases.
Paradoxically, this excess oil production ultimately reduces the lipid layer of the tear film. How? The excess
quantity of oil on the lid margin promotes the formation of a crusty debris in and around the meibomian glands
which eventually clogs the meibomian orifices, or at the very least interferes with meibomian secretions.
These oily deposits on the lid margin provide bacteria with an ideal environment for infestation and
multiplication, so it's not surprising that indigenous Staphylococcal infection often accompanies and exacerbates
seborrheic blepharitis.
In infectious blepharitis, bacterial exotoxins called lipases break down the cholesterol compounds within the
meibomian secretions. This frees fatty acids, which are directly toxic to the corneal epithelium, resulting in
punctate epitheliopathy and inflammation. Disturbance to the lipid layer increases tear evaporation and
subsequently promotes dry eye.
MANAGEMENT
The mainstay of therapy is improved lid hygiene. This alone may enable you to control symptoms and prevent
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Handbook of Ocular Disease Management - Blepharitis
further complications. Eyelid scrubs using a mild, deodorant-free soap or tearless shampoo will resolve or
ameliorate most cases. The treatment dissolves eyelash and skin debris that is often laden with bacteria.
Commercially available lid scrubs include Ocu-clear, Lids and Lashes, Lid Wipes SPF and Lid Scrub.
For moderate, severe or chronic cases, you may need to prescribe topical and/or oral medications. When
choosing medications, consider these four factors:
●
the severity of the condition
●
the effectiveness of the agent
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the potential for toxicity reactions
●
the propensity for allergic reaction
Sulfa drugs (i.e., sulfacetamide) are the classic medications for treating Staphylococcal infection. These work by
competitive inhibition of para-amino benzoic acid (PABA), which inhibits cellular processes of the bacteria.
Today, despite a reputation for broad spectrum activity, sulfa-based medications are often ineffective because
many organisms have developed resistance to sulfa drugs. In these cases, other acceptable preparations include
gentamicin, tobramicin, erythromicin and neomycin, polymyxin B and bacitracin, prescribed BID/QID in either
ointment or drop form.
If there's excessive inflammation and/or discomfort, try using an antibiotic-steroid combination prescribed BID
or QID, in either ointment or eye drop form. Acceptable choices include:
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tobramycin and dexamethasone alcohol (Tobradex)
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neomycin or polymyxin B with hydrocortisone (Cortisporin)
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neomycin or polymyxin B with dexamethasone (Maxitrol)
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sulfacetamide and prednisolone acetate (Blephamide)
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sulfacetamide & prednisolone sodium phosphate (Vasocidin)
In recalcitrant cases, try oral tetracycline, 250 to 500mg, BID or QID. While this concentration is not
bactericidal, it inhibits the bacterial production of lipases, which increases stability of the tear film.
CLINICAL PEARLS
●
If, upon digitally expressing clogged meibomian glands, the exudate appears milky white rather than
clear, the bacteria have infected the gland itself. This usually warrants oral antibiotic therapy.
●
Check patients on non-steroidal medications in seven to 10 days, and those using antibiotic-steroid
combination within three to five days, for IOP response to the steriod. Follow-up with unmedicated
patients every six months or as needed.
●
Patients with chronic or recurrent history or those who fail to respond to medical therapy may be
suffering from acne rosacea. These patients need oral antibiotics and possibly a dermatologic consult.
●
Rarely, infectious blepharitis occurs from a fungus such as Candida albicans or Aspergillus fumigatus
rather than indigenous Staphylococcal bacteria. The distinguishing factor is the presence of granulomas
in fungal infection; non-granulomatous infections are bacterial.
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Left unattended, chronic blepharitis can spawn degenerative changes in the skin (ulcerative blepharitis),
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Handbook of Ocular Disease Management - Blepharitis
meibomianitis, hordeola, chalazia and marginal sterile keratitis.
Other reports in this section
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Blepharitis
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Handbook of Ocular Disease Management - Basal Cell Carcinoma
Basal Cell Carcinoma
SIGNS AND SYMPTOMS
Basal cell carcinoma is the most common malignancy of the eyelid,
accounting for over ninety percent of all cancerous lid lesions. Often,
this tumor is discovered during routine slit lamp evaluation. There is
usually no associated pain or discomfort. Basal cell carcinoma is more
fig05.jpg (8710 bytes)
common in older, fair-skinned individuals, especially with a history of
prolonged or excessive exposure to sunlight. The lower lid margin and
medial canthus are the most common areas involved.
The basal cell lesion presents in one of three ways: (1) the nodular form appears as a small, translucent, raised
area with poorly defined edges, and is firm to the touch; (2) the classic ulcerative presentation is a nodular lesion
that over time has developed telangiectasia (a reddish hue caused by persistent, and virtually permanent, dilation
of capillaries) along the surface and an atrophied inner portion, creating a "pearly," indurated outer margin with
an excavated center; and (3) less frequently, the sclerosing or morpheaform basal cell carcinoma form, which
has a firm, pale, waxy yellow plaque with indistinct borders.
PATHOPHYSIOLOGY
While there is no single known cause for all forms, there is a distinct association with increasing age and
exposure to ultraviolet radiation. In addition, Caucasians have a much greater chance of developing basal cell
carcinoma than other races. The progression of this tumor is, in most cases, exceedingly slow. If left untreated,
however, the lesion may in time invade deeper structures. Fortunately, metastasis is rare, and complete recovery
is possible with proper therapy.
MANAGEMENT
Basal cell carcinoma can be treated with surgical excision, radiation therapy or chemotherapy. The preferred
course for most cases is surgery, with broad margins to ensure complete removal. Local radiation therapy and/or
systemic chemotherapy can manage basal cell carcinoma when surgery is intolerable or refused by the patient.
Both of these modalities carry significant side effects, however, and neither is as effective as surgical
intervention.
CLINICAL PEARLS
●
Basal cell carcinoma is rarely life-threatening because of its non-metastatic, slow-growing nature.
However, this tumor does possess the capacity, over time, to cause significant local destruction, and
must always be treated appropriately.
●
Early biopsy is often the key to diagnosis. Biopsy all suspicious lid lesions which demonstrate irregular
growth, changes in color or appearance, or purulent or bloody discharge to rule out cancer. You should
refer confirmed malignancies promptly to an oculoplastics specialist or, if possible, an ocular oncologist.
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Handbook of Ocular Disease Management - Basal Cell Carcinoma
Other reports in this section
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Basal Cell Carcinoma
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Handbook of Ocular Disease Management - Blow-Out Fracture
Blow-out Fracture
SIGNS AND SYMPTOMS
Patients manifesting orbital blow-out fracture always present with
a history of blunt ocular trauma. Blow-out fracture is usually
caused by a large, low-velocity object, such as a fist or a ball.
Sports-related injuries are common. If the trauma is recent, the
patient may present with symptoms of pain, local tenderness and
double vision. Complaints of an intense pressure feeling or
swelling of the eye associated with nose blowing may also be
reported.
Critical signs of recent blow-out fracture include:
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edema and ecchymosis of the lid tissues
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restriction of ocular motility, especially with vertical
movements
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orbital crepitus (subcutaneous emphysema)
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hypoesthesia of the ipsilateral cheek, due to entrapment of
the infraorbital nerve.
There may also be an associated nosebleed due to communication between the orbit and maxillary sinus. Orbital
edema initially surrounds and displaces the globe, in some cases causing the eye to appear proptotic. However,
as the swelling subsides, the eye is likely to drop down and back, becoming enophthalmic. Associated traumatic
uveitis and/or hyphema may be noted as well.
In some cases, patients suffering orbital blow-out fracture initially ignore treatment, and may present long after
the initial inflammatory manifestations of trauma have subsided. In these patients, evaluation reveals only
relative enophthalmos and motility restriction, usually in upgaze, and possible infraorbital hypoesthesia.
PATHOPHYSIOLOGY
Blow-out fracture may result in cases of abrupt trauma to the eye by any object >5cm in diameter. Because the
orbital rim is very strong, the forces of blunt trauma are reflected back, compressing the eye and creating a
tremendous increase in pressure within the orbit.
Since the larger bones which comprise the orbit contain sinuses, the orbital walls are at great risk for fracture;
should the trauma be of sufficient force, these walls can literally "blow out." The medial wall (ethmoid bone) is
occasionally affected. But most commonly, the orbital floor (the superior aspect of the maxillary bone) sustains
the damage. In cases of floor fractures, the eye may partially drop down into the maxillary sinus, causing
enophthalmos and entrapment of the inferior rectus or inferior oblique muscle.
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Handbook of Ocular Disease Management - Blow-Out Fracture
This entrapment leads to a tethering effect, resulting in a limited downgaze ability and, more notably, an
inability toward upgaze in the affected eye. While this situation can be surgically corrected in the early stages,
prolonged entrapment leads to fibrosis of the muscle(s) and permanent motility impairment. Associated medial
wall fractures may induce damage to the medial rectus muscle and/or the lacrimal apparatus, but this is
uncommon.
In most cases, these fractures result in orbital emphysema, creating a direct communication between the ethmoid
sinus and the orbit. This produces the feeling of pressure within the orbit when the patient attempts to blow his/
her nose. The greatest risk to consider with medial wall fractures is orbital cellulitis, secondary to sinus
infection, should pathogenic organisms within the sinus invade the post-tarsal eyelid.
MANAGEMENT
All cases of blunt ocular trauma with resultant crepitus or motility restriction warrant orbital imaging studies.
Computed tomography (CT scan) is the procedure of choice. CT is better at imaging the bony structures of the
orbit than either plain skull films (X-ray) or MRI. Obtain both axial and coronal scans.
Should you discover a floor fracture with associated herniation of the orbital contents, consider surgical
intervention. Generally, surgery is only for patients with recent trauma who manifest significant diplopia in
primary gaze or downgaze, or in cases of cosmetically unacceptable enophthalmos. Most oculoplastic specialists
will wait 10 to 14 days following the trauma to allow for resolution of the associated edema and hemorrhage.
The treatment consists of surgical resection of the periosteum and repair of the fracture, utilizing a bone graft or
synthetic material such as silicon or Teflon.
Long-standing entrapment of the extraocular muscles leads to fibrosis and irreversible scarring; intervention to
improve motility after four weeks is typically unsuccessful. Initiate prophylactic antibiotic therapy immediately
in the event of associated medial wall fractures with orbital emphysema, or if there is any suspicion of ethmoid
damage. A broad spectrum oral preparation such as cephalexin or erythromycin (250-500mg QID) may be used
for 10 to 14 days. Surgical repair of the medial wall is unnecessary in uncomplicated ethmoid fractures, since the
condition resolves spontaneously in three to four weeks.
CLINICAL PEARLS
●
Cases of orbital blow-out fracture do not constitute an emergency, however, accurate diagnosis and
management of the associated ocular manifestations is paramount.
●
One test that is very helpful in differentiating muscle entrapment in orbital fracture from other muscle or
nerve complications is the forced duction test. Entrapped muscles will resist forced movements with a
forceps or even a cotton-tipped applicator. Again, this test should ideally be performed after resolution of
the orbital swelling.
●
Check for crepitus by palpating the bony rim of the orbit or lid-small bubbles of air will "pop" when
compressed.
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For long-standing fractures in which the patient experiences diplopia in downgaze, but is not a surgical
candidate, consider incorporating unilateral prism correction into the patient's reading glasses.
Other reports in this section
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Handbook of Ocular Disease Management - Blow-Out Fracture
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Blow-out Fracture
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Handbook of Ocular Disease Management - Chalazion
Chalazion
SIGNS AND SYMPTOMS
Patients will present with one or many focal, hard, painless nodules in
the upper or lower eyelid. They may report some enlargement over time,
and there may be a history of a painful lid infection prior to the
chalazion development, but this isn't always the case. Chalazia are often
recurrent, especially in cases of poor lid hygiene or concurrent
blepharitis.
PATHOPHYSIOLOGY
A chalazion is a non-infectious, granulomatous inflammation of the meibomian glands. The nodule itself
consists of many types of steroid-responsive immune cells, including connective tissue macrophages known as
histiocytes, multinucleate giant cells, plasma cells, polymorphonuclear leukocytes and eosinophils.
A chalazion may be a residual aggregation of inflammatory cells following an eyelid infection such as hordeola
and preseptal cellulitis, or may develop from the retention of meibomian gland secretions.
MANAGEMENT
Chalazia are non-infectious collections of immune cells that require intensive steroid therapy. Because chalazia
reside deep under the skin, no topical medications will be able to penetrate sufficiently. About 25 percent of
chalazia resolve spontaneously. For those that don't, instruct the patient to apply a hot compress to open the
glands, then to digitally massage the area to break and express the nodule, up to four times a day.
If this is ineffective, inject triamcinolone acetonide (Kenalog) 5mg/ml or 10mg/ml directly into the chalazion
(some practitioners have advocated concentrations as high as 40mg/ml, but this is not standard practice).
Approach the lesion from the palpebral side, and inject 0.05 to 0.3ml in standard form, using a tuberculin
syringe and 30-gauge needle. You may want to use a chalazion clamp and topical anesthesia, but this is not
absolutely necessary. Usually the patient is markedly better one week later, but you may need to re-treat
extremely large chalazia. If the chalazia persists even after a second steroid injection, or if the patient cannot
tolerate the procedure, excise the remaining lesion using a curette under local anesthesia as a last resort.
CLINICAL PEARLS
●
Intralesional steroid injection is contraindicated for patients with dark skin, since the procedure can
cause depigmentation which often persists for months, or is permanent. This is especially likely if the
point of injection is on the skin, but may occur even if injecting through the palpebral conjunctiva.
●
Biopsy any recurrent chalazia, especially those following surgical excision, to rule out a particularly
deadly malignancy known as sebaceous gland carcinoma.
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Handbook of Ocular Disease Management - Chalazion
Other reports in this section
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Chalazion
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Handbook of Ocular Disease Management - Chronic Epiphora
Chronic Epiphora
SIGNS AND SYMPTOMS
Epiphora is more of a clinical sign than an absolute diagnosis. This
condition constitutes insufficient drainage of the tear film from the eyes.
Be aware of the distinction between chronic and acute epiphora. Chronic epiphora results from long-standing or
unremitting disorders, and presents a greater clinical challenge than acute epiphora. The acute variety most often
results from irritative ocular conditions such as corneal foreign bodies or allergic conjunctivitis, and usually
resolves with treatment of the associated disorder. Patients with chronic epiphora report excessive lacrimation,
in some cases to the point of tears actually streaming over the lid margins and down their face.
The symptoms may be exacerbated by environmental factors such as excessive cold, wind, pollen or other
airborne particulate matter, sleep deprivation, nearpoint strain, or emotional stress. Regarding the latter, some
patients may report that they "cry very easily," or that they are constantly wiping their eyes.
Often, the patient complains of intermittently reduced acuity, owing to excessive tears. Irritation to the lids, and
in particular the inner canthus, is common because of the constant wetting of that area as well as the continuous
mechanical abrasion of tissues. Punctate epithelial keratopathy is another prevalent finding in patients with
epiphora. Lid-globe appositional abnormalities, punctal stenosis and lacrimal sac disorders may also be noted.
PATHOPHYSIOLOGY
Epiphora may result from a variety of conditions, but all can be ascribed to one of four basic categories: lid-
globe appositional abnormalities, obstructive lacrimal drainage disorders, ocular surface disorders, and rarely,
neurogenic lacrimal hypersecretory disorders.
In conditions that alter the normal proximity of the lacrimal puncta to the ocular surface, outflow of tears is
impeded. The most obvious cause is acquired ectropion; other examples include entropion and floppy eyelid
syndrome.
Obstructive disorders of the lacrimal system are similar to appositional abnormalities, except that in these
conditions there is mechanical impedance of the outflow channel. This may take the form of acquired punctal
stenosis, canalicular stenosis or canaliculitis, dacryocystitis or lacrimal sac tumors. Occasionally, a large
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Handbook of Ocular Disease Management - Chronic Epiphora
hordeolum or chalazion may induce punctal or canalicular stenosis.
Ocular surface disorders can in some instances induce excessive and symptomatic reflex tearing. While this is
typically not significant enough to constitute true epiphora, it should be considered when patients present with
complaints of "excessive tearing." Disorders such as chronic keratoconjunctivitis sicca may induce reflex
epiphora, in the absence of any lid or lacrimal abnormalities.
Finally, hypersecretion of tears may be encountered in rare neurogenic disorders. Compressive irritation of the
parasympathetic lacrimal fibers or aberrant regeneration of cranial nerve VII after trauma may result in enhanced
lacrimation, sometimes referred to as "crocodile tears." Rule out neurogenic complications prior to initiating
therapy for a lacrimal outflow problem.
MANAGEMENT
Treatment for epiphora involves alleviating the symptoms and correcting the underlying disorder. For lid-globe
appositional abnormalities, such as ectropion, the only cure is to surgically realign the punctum with the globe.
In some cases of mild medial laxity with punctal eversion, the lid may be repositioned with local cautery alone.
Most often, however, this involves modified resection of the lid tissue, or "horizontal lid shortening procedures."
Obstructive disorders generally require somewhat invasive therapeutic measures as well. Punctal and/or
canalicular dilation and irrigation is the most common management for stenosis of the lacrimal system. In cases
of chronically flaccid or stenotic puncta, laser punctoplasty or ampullotomy may be used to enlarge the outflow
orifice. If the blockade exists more distally within the nasolacrimal system, probing alone may be inadequate to
alleviate the problem. In these cases, dacryocystorhinostomy (DCR) is often required; this creates a surgical
bypass of the common canaliculus directly into the nasal mucosa. Probing procedures are contraindicated in
cases of inflammation, such as chronic dacryocystitis, or suspected neoplasm; implement DCR for these
conditions.
When ocular surface disorder is the etiology of chronic epiphora, aim treatment at replenishing the normal basal
tear volume and improving the overall quality of the tear film. Use artificial tear preparations, punctal or
lacrimal occlusion therapy, moist chamber effects, or a combination of these strategies.
Neurogenic hypersecretory disorders, when suspected, should be referred for evaluation and management by a
neurologist.
CLINICAL PEARLS
●
"Tearing" is a common complaint in most optometric practices. For proper management, differentiate
between functional epiphora and occasional, symptomatic lacrimation. True epiphora constitutes a
chronic problem warranting intervention, whereas normal tearing does not.
●
Dilation and irrigation, the most common management strategy for punctal and canalicular obstruction,
is a quick and easy in-office procedure that can be performed by an optometrist. It is not a permanent
solution, however, and may need to be repeated several times each year to maximize patient comfort and
satisfaction. Surgical intervention, when necessary, should be directed to an experienced oculoplastic
specialist.
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Handbook of Ocular Disease Management - Chronic Epiphora
Other reports in this section
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Handbook of Ocular Disease Management - Dacryocystitis
Dacryocystitis
SIGNS AND SYMPTOMS
Pain, redness and swelling over the inner aspect of the lower eyelid and
epiphora may signify aggravated blepharitis, meibomianitis or
canaliculitis. However, suspect dacryocystitis if the problem recurs and
is associated with fever and severe erythematous swelling around the
nasal aspect of the lower lid; or if it involves the lacrimal sac such that
mucopurulent discharge can be expressed from the inferior punctum.
Older patients are predisposed to the condition as the lacrimal drainage
system loses its elasticity and thins, and tears fail to flush debris through
the complex. Patients with poor hygiene are at greater risk.
PATHOPHYSIOLOGY
The primary etiology of dacryocystitis is nasolacrimal obstruction secondary to mucocele of the lacrimal sac,
which is precipitated by chronic blockage of the interosseous or intermembranous nasolacrimal duct. Most cases
of nasolacrimal duct obstruction are found in the older population, and result from chronic mucosal
degeneration, ductile stenosis, stagnation of tears, and bacterial overgrowth. Infantile dacryocystitis is
uncommon but presents with the same signs and symptoms.
Lacrimal sac obstructions often produce signs and symptoms similar to dacryocystitis but not as severe. They are
collectively known as canaliculitis. These infections are differentiated by solid concretions called dacryoliths,
which can be expressed from the infected lacrimal sac. Dacryoliths can result from bacterial, fungal or viral
infections.
MANAGEMENT
Management of an afebrile child with dacryocystitis includes oral amoxicillin/clavulanate (Augmentin) 20-
40mgs/kg/day, PO, TID, or oral cefaclor 20-40mgs/kg/day, PO, TID, along with topical antibiotic drops QID (e.
g. Polytrim, Tobrex, Ocuflox), ointments BID, warm compresses and acetaminophen. Management of an adult
afebrile patient includes cephalexin (Keflex) or Augmentin 500mgs PO, QID along with topical antibiotic drops,
ointments, warm compresses and aspirin or ibuprofen for pain and inflammation, as needed. Manage febrile
patients with extreme caution. Patients who are acutely ill should be hospitalized and placed on IV cefazolin
(Ancef), Q8H along with the other modalities. Consider neuroimaging (CT or MRI) when the etiology is in
question.
Dacryoliths should be removed with curettage or canaliculotomy, cultured and treated accordingly with both
topical and oral antibiotic, antiviral or antifungal preparations.
CLINICAL PEARLS
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Handbook of Ocular Disease Management - Dacryocystitis
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Obstruction of the tear drainage system can occur at any age. Punctal or canalicular stenosis may
develop from a myriad of conditions. Punctal stenosis may result from conjunctival diseases such as
Steven's-Johnson syndrome (dry eye and dry mouth secondary to reaction to sulfa medicine), ocular
cicatricial pemphigoid, and mechanical, thermal or chemical injury. In the young, congenital anomalies
of the nasolacrimal system include dacryostenosis, dacryocystocele and canalicular fistula
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Bloody tears with a history of medial canthal mass should heighten suspicion for space occupying
lesions. Facial cellulitis and acute ethmoidal or frontal sinusitis are among the important differential
diagnoses.
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Prompt, decisive and aggressive management is essential. Hospitalization with intravenous antibiotics
should be considered in severe, febrile or recalcitrant presentations. Punctal dilation and nasolacrimal
irrigation is always contraindicated in the acute stages. In fact, following the resolution of the acute
infection, most cases remain with symptomatic epiphora, requiring dacryocystorhinostomy.
Other reports in this section
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Handbook of Ocular Disease Management - Herpes Simplex Blepharitis
Herpex Simplex Blepharitis
SIGNS AND SYMPTOMS
Signs and Symptoms: Herpes simplex virus (HSV) infections
involving the lid may present in one of two forms. The classic
appearance involves an accumulation of small vesicles or
pustules along the lid margin and/or periocular skin. These
01a.jpg (20127 bytes)
lesions typically have an inflamed, erythematous base. Within
the first week of infection, the vesicles may ulcerate or harden
into crusts.
A second “erosive-ulcerative” form of HSV blepharitis has also been described. This presentation is
characterized by erosions of the lid at the Gray line or ulcers along the lid margin, or a combination of both.
The lid typically displays generalized swelling and redness associated with these lesions.
HSV blepharitis is encountered primarily in children, although adults may also manifest this disorder.
Presenting symptoms include pain and tenderness upon palpation, as well as increased lacrimation in severe
cases. If the conjunctiva is involved, tarsal follicles may be observed along with bulbar injection and chemosis.
Swollen pre-auricular nodes (pre-auricular lymphadenopathy) on the involved side is common.
PATHOPHYSIOLOGY
Herpes simplex is actually the most common virus found in humans. A member of the Herpetoviridae family,
HSV is a double-stranded DNA virus that replicates within cell nuclei. As it leaves the host cell, it becomes
encapsulated and can lie dormant for extended periods. Several trigger factors, including fever, trauma,
emotional stress, menstruation, exogenous immunosuppressive agents, and overexposure to UV radiation can
activate the virus. Transmission typically occurs by direct contact with an open epithelial lesion or
contaminated bodily secretions. Rarely, the virus may be spread by contaminated materials such as towels or
tissues.
Primary ocular infections occur most often in children between the ages of 6 months and 5 years, and almost
invariably present as blepharitis or blepharoconjunctivitis. In recurrent attacks, the virus usually reappears as a
dendritic keratitis. Several reports of recurrent HSV blepharitis have been reported in the literature, however.
MANAGEMENT
There is no specific treatment for HSV blepharitis, and most often the course of the disease is self-limiting. The
use of warm saline compresses with a topical drying agent (e.g. 70% alcohol) is usually sufficient to palliate the
patient. If the lesions are extensive, concomitant use of topical antibiotic ointment is prudent to prevent a
secondary opportunistic bacterial infection. The use of topical or oral antiviral agents has not been proven to
enhance the recovery of patients with HSV blepharitis, although it is advocated by some practitioners for more
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Handbook of Ocular Disease Management - Herpes Simplex Blepharitis
severe cases. However, topical trifluridine (Viroptic 1%) is absolutely indicated in cases presenting with
corneal involvement.
The use of topical steroids on HSV lid lesions may be unwise, particularly if there is other ocular involvement.
Although corticosteroids may be used without fear in cases of herpes zoster (HZO) blepharitis, their use in
cases of HSV infection may predispose the patient to the eruption of a dendritic keratitis.
CLINICAL PEARLS
• Always include HZO in the differential diagnosis of HSV blepharitis. Keep in mind, however, that HZO
typically affects elderly patients over the age of 70. Younger patients who present with HZO are often
immunocompromised secondary to disorders such as AIDS or lymphoma. HSV blepharitis is usually
encountered in children, but can occur at any age.
• Although herpes simplex is known as a sexually transmitted disease, the vast majority of ocular herpes
infections are not contracted via sexual contact. This is very important to recognize when considering pediatric
cases of HSV blepharitis.
Other reports in this section
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Herpes Simplex Blepharitis
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Handbook of Ocular Disease Management - Herpes Zoster Ophthalmicus
Herpes Zoster Ophthalmicus
SIGNS AND SYMPTOMS
Herpes zoster ophthalmicus (HZO) typically presents with nondescript
facial pain, fever and general malaise. About four days after onset, a
vesicular skin rash appears along the distribution of the fifth cranial
nerve, characteristically respecting the vertical midline. The vesicles
will discharge fluid and begin to scab over after about one week. The
pain is extreme during the inflammatory stage, and patients are
tremendously symptomatic.
Ocular involvement may include follicular conjunctivitis, epithelial and/or interstitial keratitis, dendritic
keratitis, uveitis, scleritis or episcleritis, chorioretinitis, optic neuropathy, and even neurogenic motility disorders
(especially fourth cranial nerve palsy). If you see vesicles at the tip of the nose (known as Hutchinson’s Sign),
there is a 75 percent likelihood of ocular sequelae.
PATHOPHYSIOLOGY
HZO occurs when the trigeminal ganglion is invaded by the herpes zoster virus, a varicella-type virus which is
usually referred to as “chicken pox” in children or “shingles” in adults. The virus remains dormant in trigeminal
nerve cells, and can become reactivated years later by a reduction in the immune system.
Neuronal spread of the virus occurs along the ophthalmic (1st) and less frequently the maxillary (2nd) division
of the fifth cranial nerve. Vesicular eruptions occur at the terminal points of sensory innervation, causing
extreme pain. Nasociliary involvement will most likely cause ocular inflammation, typically affecting the tissues
of the anterior segment. Contiguous spread of the virus may lead to the involvement of other cranial nerves,
resulting in optic neuropathy (cranial nerve II) or isolated cranial nerve palsies (cranial nerve III, IV or VI).
MANAGEMENT
The systemic component of this disorder is best treated with oral acyclovir, (Zovirax), 600 to 800mg five times a
day for seven to 10 days, starting as soon as the condition is diagnosed. Recently, famciclovir (Famvir) 500mg p.
o. t.i.d. has been shown to be as effective in treating herpes zoster ophthalmicus as acyclovir 800mg fives times
per day. Timing is crucial, however, to avoid post-herpetic neuralgia. To achieve maximal benefit from oral anti-
viral medications, you must start therapy within 72 hours of vesicular eruption. Otherwise, the patient is at risk
for developing post-herpetic neuralgia and the beneficial effects of oral anti-viral therapy are lost. You may also
wish to prescribe oral steroids to alleviate pain and associated facial edema. If so, try 40 to 60mg of prednisone
daily, tapered slowly over 10 days. To treat the skin lesions, applying an antibiotic-steroid ointment, such as
Pred-G, to the affected areas twice daily, may help.
Ocular management depends on the severity and tissues involved. In most cases which involve uveitis or
keratitis, use cycloplegia (homatropine 5% t.id./q.i.d. or scopolamine 0.25%) b.i.d./q.i.d. After ruling out herpes
simplex, it’s also possible to prescribe a topical steroid such as Vexol or Pred Forte q2-q.h. In any compromised
eye, prophylaxis with a broad-spectrum antibiotic is a good idea. Finally, palliative treatment consisting simply
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of cool compresses, and oral analgesics in extreme cases, can be comforting. Cimetidine 400mg p.o. b.i.d may
provide some additional relief from the neuralgia; why this works is not entirely understood.
CLINICAL PEARLS
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People over age 70 have a much greater chance of HZO infection. Also, those who are
immunocompromised due to lymphoma, AIDS, Lyme disease, etc. are at an increased risk.
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Ocular involvement varies greatly and is often confusing in the early stages.
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Take extreme care when differentiating this condition from herpes simplex virus (HSV), particularly
when there is corneal involvement. One key consideration is that the dendritic keratitis which occurs in
HZO is infiltrative, while the HSV dendrites are ulcerative.
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Also keep in mind the possibility of more involved and complex ocular sequelae (chorioretinitis, optic
neuropathy, cranial nerve palsies, uveitic glaucoma), and apply appropriate management strategies in
these cases.
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Start oral anti-viral therapy within 72 hours of vesicular eruption to possibly avoid post-herpetic
neuralgia.
Other reports in this section
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Herpes Zoster Ophthalmicus
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Handbook of Ocular Disease Management - Hordeolum
Hordeolum
SIGNS AND SYMPTOMS
Patients will present with an acutely swollen and edematous upper or
lower eyelid. Visual function will be normal. There may be an
associated conjunctivitis and possibly mucopurulent discharge. The lids
will be extremely sensitive to palpation, and there may be an associated
pustular, pimple-like lesion at the lid margin or, less commonly, at the
dermis.
PATHOPHYSIOLOGY
A hordeolum is a bacterial infection of either the meibomian glands or ciliary glands (the glands of Zeis and
Moll). If the latter are involved, the hordeolum is considered external and appears focal in nature. If the deeper
meibomian glands are involved, the hordeolum is considered internal and is less circumscribed in appearance.
Staphylococcus aureus and Staphylococcus epidermidis are the most likely culprits. Acute and chronic
inflammation associated with hordeola, especially if improperly treated, may result in a granulomatous
inflammation known as chalazia. If the infection spreads to neighboring glands or other lid tissue anterior to the
tarsal plate, it may lead to preseptal cellulitis.
MANAGEMENT
Traditionally, the standard treatment has been topical antibiotic solutions and ointments. Unfortunately, this has
virtually no therapeutic benefit. Topical application does not supply enough intra-tissue concentrations of
antibiotics to be effective. Oral antibiotic therapy is necessary. If the hordeolum is external, you may drain and
lance the lesion (anesthetic is usually unnecessary) or epilate nearby lashes to enhance drainage. Digital
expression of purulent material in your office will expedite healing, but is not absolutely necessary. Antibiotic
therapy could include dicloxacillin 250mg PO Q6H, erythromycin or tetracycline 250mg PO QID or
amoxacillin 500mg PO TID for 10 days. Cold compresses will help to suppress inflammation.
CLINICAL PEARLS
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The most common misdiagnosis of hordeola is chalazia. The distinguishing factor is pain upon
palpation. If the lesion is not intensely sensitive to palpation, most likely it's a chalazion.
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Avoid traditional topical therapies, which are therapeutically ineffective, and begin immediately with
oral medications.
Other reports in this section
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Hordeolum
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Handbook of Ocular Disease Management - Hordeolum
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Handbook of Ocular Disease Management - Molluscum Contagiosum
Canaliculitis
Signs and symptoms: Canaliculitis is a relatively rare disorder
that predominantly affects individuals over age 50. Complaints
center on a chronic, recalcitrant unilateral red eye, and often
epiphora. The discharge may range from a simple watery
fig01.jpg (5755 bytes)
consistency to full-blown mucopurulence. In many cases, the
patient will report previous therapy with topical antibiotics, but to
no avail. Recurrent episodes are not uncommon.
Biomicroscopic inspection reveals a classic "pouting punctum" in
Canaliculitis.
the involved eye--that is, the punctal orifice is red, swollen and
turned outward, like pouting lips. The involved area is often tender to touch. Digital manipulation of
the punctum and/or canaliculi may express discharge and/or concretions. Other important signs
include erythema and swelling of the lid and adnexal tissue, and a conjunctivitis that is most
pronounced inferiorly and nasally.
Lacrimal probing reveals additional diagnostic signs. You will encounter a "soft stop" while probing the
canaliculus. This blockage indicates the presence of concretions within the drainage system.
Concurrent with this finding is the so-called "wrinkle sign"; as your probe meets resistance, the
overlying skin of the medial canthus may compress and wrinkle. The Jones test for fluorescein dye
disappearance is inherently negative.
Pathophysiology: Canaliculitis results from an infection of the canaliculus. Most often a bacterial
pathogen causes this, though it can also result from fungal or viral infection. In older individuals,
Actinomyces israelii is the primary etiology. Those under age 20 who present with canaliculitis are
more likely to manifest primary herpetic infections. Other less common etiologies include
Fusobacterium, Nocardia, Candida, Fusarium and Aspergillus species.
Infections within the canaliculi cause dacryoliths--small stones or concretions that further impede
lacrimal drainage--to form. These concretions help to form "pockets" in which the infection flourishes,
not subject to the antimicrobial properties of the precorneal tear film. Foreign bodies that lodge within
the canaliculus can produce a similar presentation.
Management: Management of canaliculitis is twofold, consisting of physical removal of associated
foreign matter and vigorous antimicrobial therapy. Small dacryoliths and other debris may be
expressed through the punctum with direct manipulation using a cotton-tipped applicator. Larger or
numerous stones often require surgical canaliculotomy.
Institute antimicrobial therapy only after alleviating the blockage. Treatment options depend on the
offending agent. Obtain smears and cultures from the extruded canalicular material. In cases of
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Handbook of Ocular Disease Management - Molluscum Contagiosum
bacterial infection, irrigate the canaliculus with penicillin G solution (100,000 units/ml). Usually, you
will then follow-up with topical therapy (Polytrim or Neosporin ophthalmic solution) and systemic
antibiosis (penicillin or ampicillin) for 1-2 weeks. Treatment for herpetic infection consists of topical
trifluridine 1% five times daily for 2-3 weeks. Address fungal infections by using nystatin 1:20,000
ophthalmic solution tid, as well as biweekly nystatin irrigation.
Clinical Pearls:
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Differentiate canaliculitis from dacryocystitis; the latter presents more acutely and with greater
pain and swelling in the canthus region.
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Herpetic canaliculitis often follows herpes simplex blepharoconjunctivitis. Consider this in
cases that manifest persistent epiphora after resolution of the herpes vesicles.
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If treatment fails to eradicate the problem, or if canalicular patency cannot be restored, a
dacryocystorhinostomy may be required.
Other reports in this section
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Canaliculitis
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Handbook of Ocular Disease Management - Pediculosis & Phthiriasis
Pediculosis & Phthiriasis
SIGNS AND SYMPTOMS
Pediculosis is an eyelid infestation by either Pediculus humanus corporis
(body) or Pediculus humanus capitus (head). Phthiriasis, which is
actually the most common eyelid infestation, is caused by Phthirus pubis
(pubic lice, sometimes referred to as crab lice).
fig07.jpg (10129 bytes)
Pediculus are 2 to 4 mm long, and typically infest the hair of the patient. Infestation of the cilia is rare and only
occurs in the worst cases. Phthirus are 2mm long, and have a broad-shaped, crab-like body. Its thick, clawed
legs make it less mobile than the Pediculus species and lend it to infesting areas where the adjacent hairs are
within its grasp (eyelashes, beard, chest, axillary region, pubic region). They rarely infest the scalp.
Ocular signs and symptoms include visible organisms on the scalp, hair, eyelashes or beard; visible blue skin
lesions (louse bites); reddish brown deposits (louse feces); secondary blepharitis with preauricular adenopathy;
follicular conjunctivitis; and, in severe cases, marginal keratitis. The patient often complains of bilateral ocular
itching and irritation.
PATHOPHYSIOLOGY
The Pediculus and Phthirus organisms look similar the each other and interbreed freely. Both types lay eggs on
the hair shafts and remain firmly adherent, resisting both mechanical and chemical removal. The Pediculus
organism moves well and can be passed from person to person by either close contact or by contact with
contaminated bedding. Conversely, Phthiriasis are slow moving, and cannot typically be passed unless cilia is
brought into close proximity with infested cilia. Both species are associated with crowded conditions or poor
personal hygiene.
MANAGEMENT
Begin management by removing all visible organisms and nits (eggs) with forceps. Place the removed debris in
an alcohol wipe and discard it promptly. Instruct the patient to use a pediculocidic-medicated shampoo such as
Rid (a safe, effective, non-prescription pediculoside), Lidane 1% (gamma benzene hexachloride), Permethrin
1%, A-200 Pyrinate (pyrethrins, piperonyl butoxide, kerosene), Kwell or Nix.
Topical ocular therapy may include any of the following:
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smothering the lice and nits with petroleum jelly or other bland ointments, TID
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mercuric oxide 1% or ammoniated mercuric oxide 3%, BID
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cholinesterase inhibitors such as physostigmine
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Typically, the nits will survive a single application of these agents.
CLINICAL PEARLS
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Daily follow up is required for seven to ten days, as nits hatch every seven to ten days.
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Instruct patients to thoroughly wash all clothing and linens that may have been exposed to the organism,
and educate patients about the transmission of the disease, advising them to refrain from interpersonal
contact until the disease is 100 percent resolved. Also counsel patients to educate their recent sexual
partners about possible exposure.
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Due to ocular toxicity, pediculocide shampoos cannot be used to remove organisms from the eyelid.
Other reports in this section
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Handbook of Ocular Disease Management - Preseptal Cellulitis
Preseptal Cellulitis
SIGNS AND SYMPTOMS
Patients with preseptal cellulitis will present with an acutely painful,
swollen eyelid. Because of the pronounced edema, the patient may not
be able to open his or her eyes. However, there will be no disturbance in
fig03.jpg (6369 bytes)
visual acuity or ocular motility, nor any signs of proptosis. There may
be a concurrent history of sinus infection or congestion, penetrating
trauma to the eyelid, or dental infection. In most cases, the patient will
be systemically well and afebrile (not feverish).
PATHOPHYSIOLOGY
The eyelid is separated into preseptal and postseptal areas by the orbital septum, which prevents the spread of
infection to the orbit and central nervous system. Preseptal cellulitis is a bacterial infection of the eyelid anterior
to the orbital septum. The routes of infection include direct inoculation from trauma, or spread of infection from
the neighboring ethmoid sinus or teeth.
The most commonly encountered organisms include Staphylococcus aureus, Streptococcus pyogenes and
Streptococcus pneumoniae. If a human or animal bite wound is the source, suspect anaerobic bacteria such as
Peptostreptococcus and Bacteroides. If the infection spreads posterior to the orbital septum, it may result in a
postseptal (or orbital) cellulitis, with associated vision loss, ocular motility restrictions and proptosis. Patients
with orbital cellulitis are systemically ill and febrile.
MANAGEMENT
To prevent the possibly disastrous spread of infection to the postseptal area, it is crucial to quickly suppress the
infection. Oral therapy is necessary; topical antibiotics alone are insufficient. Amoxicillin 500mg PO TID is an
excellent choice, although you may substitute nafacillin, oxacillin or cefazolin. If the cause is a bite wound,
consider ampicillin or clindamycin. In cases of concurrent sinus infection, you may wish to consult an
otolaryngologist to help you identify the involved organism.
CLINICAL PEARLS
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Often, insect bites can mimic preseptal cellulitis, but these are rarely infectious. Instead, the patient will
have a severe local allergic reaction. If the lid is not extremely painful upon palpation, it is usually an
insect bite. A short course of oral antihistamines or steroids and cold compresses will often be sufficient.
If you are in doubt as to the infectious nature of an insect bite, proceed with oral antibiotic therapy as
well.
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occurs in adolescent viral infections such as mumps, influenza and measles.
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Handbook of Ocular Disease Management - Preseptal Cellulitis
Other reports in this section
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Handbook of Ocular Disease Management - Verruca and Papilloma
Verruca and Papilloma
Signs and symptoms: The term papilloma refers to a benign
epithelial lesion of either the skin or mucosa. Papil-lomas affecting
the eye primarily appear on the skin of the eyelid, but occasionally
they may develop on the palpebral and bulbar conjunctivae. All
fig01.jpg (5755 bytes)
papillomas have a characteristic configuration of lobular
projections that can resemble mulberries or cauliflower. They may
be flat or planar, or pedunculated. They may present singly or in
multiple numbers.
Verruca plana.
Verrucae are papillomas of viral origin. They are sometimes
referred to in the literature as viral papillomas, verruca vulgaris or
viral warts. Verrucae may vary in pigmentation from yellow to pink
to dark-brown or even black. At least two types of verrucae may
be identified clinically. Verruca plana are generally round, flat-
topped, slightly elevated lesions. Their surface is remarkably
smooth compared with other papillomas. Verrucae digitata, as the
name implies, present with numerous "finger-like" projections from
a larger base.
Papilloma.
Close inspection reveals that all verrucae are comprised of multiple filliform stalks of fibrovascular
tissue. Often there are tiny red or black dots near the surface of these projections, representing
thrombosed, dilated capillaries. Verrucae of the lids may become quite large, often becoming
keratinized over time; associated cutaneous horns are not uncommon. Verrucae of the conjunctiva
are less common and tend to maintain a more "fleshy" appearance.
Squamous papilloma is a generic term for any papilloma of non-viral origin. Most often these lesions
represent a benign dermatological condition known as acrochordon, or "skin tag." Clinically,
squamous papillomas present as round or oval, multilobular lesions. They may be sessile (attached
by a base) or pedunculated, and like verrucae they may vary in pigmentation. Most commonly, the
coloration approximates that of the patient's skin. Upon close examination, you may note a central
vascular core to each lesion, which provides blood to the proliferating epithelium. The surface is
typically roughened or granulated, reflecting the redundant epithelial cell growth.
Patients with verrucae tend to be typically between ages 5 and 20;
fewer than 15% of patients are over 35.1 Squamous papilloma, on
the other hand, is more common in those 30 and older, and the
incidence increases with age. Patients with papillomas rarely
present with symptoms beyond cosmetic concern, although in rare
instances large lesions may induce mild lid dysfunction or
discomfort. Patients who attempt to remove these lesions by
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Handbook of Ocular Disease Management - Verruca and Papilloma
picking at them may develop secondary, localized bacterial
infections.
Pathophysiology: Papillomas represent benign overgrowths of
normal epithelium, with varying levels of keratinization and
pigmentation. Histopathologically, the lesions consist of multiple
epithelial projections, the cores of which are vascularized, fibrous
connective tissue. These are covered by acanthotic (the thickened
Conjunctival caruncular papilloma. prickle-cell layer of the skin) and hyperkeratotic epithelium.
Verrucae arise from viral infection, their cores representing inflammatory hypertrophy of tissue with
viral inclusions. The causative agent in these lesions is the human papillomavirus (HPV), a double-
stranded, non-enveloped DNA virus that is spread by direct contact. As with many viral diseases,
immunocompromised patients are more susceptible to infection.
Squamous papillomas may have numerous etiologies, but most often they arise de novo as a normal
senescent skin change. The onset is gradual rather than sudden. Lesions tend not to resolve
spontaneously. Squamous papillomas may in rare instances represent precancerous lesions, so
malignant conversion remains a consideration.
Management: Given their benign nature, both verruca and squamous papillomas warrant
intervention only in cases of cosmetic concern, impaired lid function or discomfort. Obviously, if any
signs of malignancy develop, biopsy and removal are essential. Typical management involves only
patient reassurance, photodocumentation and periodic observation.
When warranted, papillomas may be removed via several methods. Less-invasive measures involve
chemical cauterization and electrocautery. The former calls for applying bichloracetic acid to the
surface of the lesion after coating the surrounding skin with petroleum ointment. This does not require
injectable anesthetic, and results in necrosis and regression of the lesion within a week to 10 days.
Electrocautery achieves the same effect, but it requires local anesthesia, and recurrence rates tend to
be higher. Obviously, neither method is suitable for lesions on the lid margin or conjunctival surface,
because of the risk to the ocular surface.
CO2 laser ablation can effectively remove lid papillomas. Most oculoplastic surgeons, however, opt for
local surgical excision, the quickest and easiest way to permanently remove these lesions. Bleeding
is the most significant problem, although topical astringents (for example, aluminum chloride) can
help achieve hemostasis. Physicians must take care when surgically removing verrucae to prevent
spread of the virus that can occur by cutting across the stalk of pedunculated lesions. The virus may
also spread if not enough of the adjacent tissue is removed.
Clinical Pearls:
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While the nomenclature regarding papillomas is sometimes confusing, it is important to
remember that these are all benign epithelial lesions. Whether the origin is hyperplasia or viral
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infection, recognition and differentiation from malignant skin lesions is the first concern. Red
flags for malignancy include: asymmetrical shape, irregular borders, abrupt changes in color or
size, and crusting or bleeding with minimal manipulation.
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Most commonly these lesions represent a purely cosmetic concern or are discovered on
routine examination. Treatment is rarely indicated, although it should be offered if the patient is
symptomatic.
●
Advise patients of the infectious nature of verrucae. These may spread to form satellite lesions
around the eye, affect skin in different regions of the body, or be transferred to other
individuals. Also realize that HPV may be spread by sexual contact. Ask patients if there are
similar lesions elsewhere on the body, and if so refer the patient for a dermatologic
consultation.
1. Odom RB, James WD, Berger TG. Andrew's Disease of the Skin: Clinical Dermatology, 9th ed.
Philadelphia: WB Saunders 2000:509.
Other reports in this section
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Verruca and Papilloma
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Orbital Cellulitis
Orbital Cellulitis
SIGNS AND SYMPTOMS
The patient with orbital cellulitis may be of any age or sex. There will be
noticeable lid edema and redness, distention, proptosis, and significant
pain upon palpation. Additionally, there will be diplopia from
extraocular motility limitations. There typically will be a precipitating
factor such as penetrating lid trauma, mucormycosis, orbital medial wall
blow-out fracture, severe lid infectious disease, bite wounds, meningitis,
sinusitis and sinus infection, septicemia, ketoacidosis, or dental abscess.
Vision loss and an afferent pupil defect may often be present. The
patient will also be systemically ill and have a fever.
PATHOPHYSIOLOGY
Orbital cellulitis results from microbial infection with subsequent inflammation of the post-septal aspect of the
eyelids. The most common routes of infection are from adjacent sinuses or teeth, and direct inoculation through
penetrating lid injury. Common organisms include Staphylococcus aureus, Streptococcus pyogenes,
Streptococcus pneumoniae, and Haemophilus influenzae in children. There is significant potential morbidity and
even mortality as a post-septal lid infection can spread through a valveless venous system leading to cavernous
sinus thrombosis, meningitis, intracranial infection, and septicemia.
Inflammatory proptosis develops due to intraorbital abscesses of mucopurulent material. Ophthalmoplegia
develops as a result of toxic myopathy and soft tissue edema. Vision loss will occur due to intraorbital increase
in pressure from the mucopurulent abscess, compressing the optic nerve.
MANAGEMENT
Differentiate orbital cellulitis from pre-septal cellulitis so as to recognize a medical emergency. There are many
superficial similarities between the two diseases, namely lid edema and redness, and pronounced pain upon
palpation. However, orbital cellulitis manifests proptosis and extraocular muscle restriction, whereas pre-septal
cellulitis does not. Also, patients with orbital cellulitis have fever and typically manifest decreased vision; these
features are not present in pre-septal cellulitis.
Often, the degree of proptosis in orbital cellulitis cannot be readily appreciated due to the extreme lid edema. For
this reason, CT scans are necessary, not only to identify orbital abscesses, but also to ascertain precipitating
sinus involvement.
There is no place for topical or oral antibiotic therapy in the management of orbital cellulitis. Optimal
management involves immediate consultation with and referral to a primary care physician, pediatrician, or
infectious disease specialist. This is especially important with children as the potential for mortality is great. The
patient needs immediate hospitalization with in-patient parenteral antibiosis.
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Orbital Cellulitis
CLINICAL PEARLS
●
When encountering a suspected orbital cellulitis, look for precipitating factors such as sinus infection,
bite wounds, dental abscess, and penetrating injury.
●
Orbital cellulitis is a medical emergency and requires in-patient care.
●
Patients with orbital cellulitis are systemically ill. The presence of fever is highly diagnostic of post-
septal orbital cellulitis. Patients who are (tentatively) diagnosed with pre-septal cellulitis should be
educated about the seriousness of the development of fever.
●
Post-septal orbital cellulitis will have motility restriction whereas pre-septal cellulitis will not.
Other reports in this section
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Orbital Cellulitis
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Senile Entropion
Senile Entropion
Signs and Symptoms
Entropion is defined as inversion of the eyelid margin. The
phenomenon may occur unilaterally or bilaterally. Although it
may involve the upper or lower eyelid, the lower lids are
affected more frequently. Clinical features associated with
entropion may be observed both in and out of the
biomicroscope and include in-turning of the eyelid margin,
eyelid skin or eyelashes contacting the cornea creating ocular
irritation, foreign body sensation, epiphora, conjunctival
hyperemia, superficial punctate epitheliopathy and, in severe or
untreated cases, corneal ulceration.
Pathophysiology
Etiologically, there are four classifications of entropion: senile (or involutional), congenital, cicatricial, and
spastic.
Senile entropion is considered to be the most common form. The lower eyelid turns toward the globe because of
increased horizontal lid laxity, an over-riding preseptal orbicularis, disinserted or atrophied lid retractors or
tendons, and involutional enophthalmos.
Congenital entropion typically effects the upper eyelid and results from structural defects in the tarsal plate,
shortened posterior lamellae (tarsal plate and conjunctiva), or eyelid retractor dysgenesis. Epiblepharon (a fold
of skin that overlaps the eyelid margin pushing the eyelid margin inward), prominent epicanthus (a fold of skin
partially covering the inner canthus, caruncle and plica semiluminaris) and microophthalmos are factors as well.
Cicatricial entropion is produced when there is as a vertical shortening of the tarsus secondary to scarring of
ocular tissue brought about by disorders such as Stevens-Johnson syndrome, ocular cicatricial pemphigoid,
trachoma, herpes zoster, trauma, chemical injuries, or thermal burns.
Spastic entropion occurs secondarily to neurologic, inflammatory or irritative processes of the eyelids.
Blepharospasm and involutional changes following surgery are among the common sources.
Management
While the treatment of choice should be guided by the underlying cause, the fundamental philosophies of
management include moving the lid margins and lashes away from the cornea and lubricating and providing
antibiotic coverage for a compromised epithelium. Generally, copious artificial tear drops and ointments can be
combined with bacitracin or erythromicin ointment, b.i.d. to q.i.d., in all cases.
Solutions for senile or involutional entropion includes eyelid retraction via taping, thermal cautery or Quickert
suture placement (a 2 to 3mm double nylon suture placed into the eyelid 2 to 3mm below the lid margin,
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Senile Entropion
perpendicular to the lid margin causing the lid to rotate away from the cornea). Other more complicated surgical
solutions exist and should referred to the ocular plastic surgeon. Botulinum toxin injection has been
demonstrated as a highly effective alternative to lid taping for temporary eyelid reposition in patients awaiting
surgery.
In cicatricial cases, surgical repair may include excision of the scar with a tarsal plate graft from preserved
sclera, ear cartilage or hard palate (in most severe circumstances) along with conjunctival and mucous
membrane grafting using fetal amniotic membrane tissue.
The easiest way to resolve spastic entropion is to remove the offending irritant. In cases that involve the seventh
cranial nerve (essential blepharospasm, orofacial dyskinesia, hemifacial spasm, facial myokymia) a neuro-
ophthalmic consult is indicated. In some instances these conditions can be managed pharmacologically using
anti-seizure medications.
Congenital cases rarely improve on their own and almost always require surgical correction. In cases such as
these, a specialist with experience in pediatric oculoplastics is preferred.
Clinical Pearls
●
A thorough history should be completed on all patients with entropion. Take note of previous eye surgery, trauma, chemical injury,
chronic infection and changes in eyelid tonus.
●
Diagnose entropion by examining the tonus of the eyelid. A sagging lower lid margin, a positive snap back test (the eyelid is loose and
snaps back poorly when pulled away from the globe), loose medial and lateral canthal tendons, and an unusually deep inferior fornix
indicate the potential for lid to globe congruity problems.
●
The differential diagnosis of entropion includes eyelash anomalies such as trichiasis (inward turning of the cilia) and distichiasis
(multiple rows of eyelashes), neuro-ophthalmic blepharospasm, traumatic etiologies, scarring from chemical injuries, and lid
malposition secondary to previous ocular surgeries.
Other reports in this section
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Senile Entropion
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Senile Entropion
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Squamous Cell Carcinoma
Squamous Cell Carcinoma
Signs and Symptoms
Squamous cell carcinoma is the second most common
malignant eyelid neoplasm in the United States, after basal cell
carcinoma.
It is most often encountered in elderly, fair-skinned individuals who have a history of chronic sun exposure.
Patients presenting with this lesion may demonstrate a roughened scaly patch of tissue on or near the lid margin
or in the canthal region. The area is typically red, elevated and nodular, with crusted and/or bloody margins.
Often, patients describe this lesion as “a non-healing scab.” According to one study, the most common
presentation involves nodular ulceration as the disease progresses, resulting in hemorrhagic or purulent
discharge.
Squamous cell carcinoma in its early stages is easily confused with a multitude of other eyelid lesions, both
malignant and benign. Some of these lesions include basal cell carcinoma, sebaceous gland carcinoma, follicular
keratosis, actinic keratosis, seborrheic keratosis, and keratoacanthoma.
Rarely are patients with squamous cell carcinoma symptomatic, displaying only mild irritation in most cases.
Acuity is not affected unless the lesion is so large as to obscure the visual axis.
Pathophysiology
Squamous cell carcinoma is a potentially invasive tumor derived from surface epithelium. In the early stages, the
normal epithelial cells are replaced by atypical squamous cells throughout the epidermis, resulting in a loss of
normal maturation. This stage is sometimes referred to as squamous cell carcinoma in situ. After the dysplastic
squamous cells encroach beyond the borders of the basement membrane, the lesion is referred to as invasive
squamous cell carcinoma.
While no single causative agent for the development of squamous cell carcinoma has been identified, it is clear
that ultraviolet radiation is a substantial risk factor and demonstrates a distinct association with this disease. This
is supported by the fact that the majority of squamous cell tumors arise on the lower lid margin and medial
canthus, the two periocular areas most susceptible to sunlight exposure. Increasing age and northern European
descent are two other commonly associated factors in patients with squamous cell carcinoma.
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Squamous Cell Carcinoma
Management
The management of squamous cell carcinoma is virtually identical to that of basal cell carcinoma of the lid.
These lesions may be treated with surgical excision, radiation therapy, chemotherapy, or cryotherapy. The
preferred course for most cases is surgery, with broad margins to ensure complete removal. Frozen tissue
sections of the tumor borders are evaluated intraoperatively to further assure that the lesion is excised
completely (Mohs micrographic technique). This method offers the greatest success with the least incidence of
recurrence. Local radiation and/or systemic chemotherapy may be used in managing squamous cell carcinoma
when surgery is intolerable or refused by the patient. Both of these modalities carry significant side effects, and
neither is as efficacious as surgical intervention. Cryotherapy has been used somewhat effectively for smaller
tumors, but does not ensure complete tumor eradication, and therefore results in a high recurrence.
Clinical Pearls
●
Squamous cell carcinoma represents approximately
●
5 percent of all eyelid malignancies. While this particular neoplasm does possess the ability to invade
local tissues and metastasize to other organ systems, it is not a particularly aggressive tumor. Its rate of
development is quite slow, and metastasis is exceedingly rare. Still, the potential for damage exists in
cases where diagnosis and treatment are delayed.
●
Early biopsy is often the key to diagnosis. Suspicious lid lesions, which demonstrate irregular growth,
changes in color or appearance, or discharge of a purulent or bloody nature should be biopsied to rule out
cancerous entities. Confirmed malignancies should be referred promptly for treatment by an
oculoplastics specialist or, where possible, an ocular oncologist.
Other reports in this section
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Squamous Cell Carcinoma
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Squamous Cell Carcinoma
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Handbook of Ocular Disease Management - Floppy Eyelid Syndrome
FLOPPY EYELID SYNDROME
Signs and Symptoms
Floppy eyelid syndrome (FES) is a relatively uncommon ocular
condition characterized by flaccid, easily everted upper lids. It is
usually seen in overweight, middle-aged males, although it may
occasionally be encountered in women and non-obese
individuals. A fair percentage of these patients also suffer from
obstructive sleep apnea (OSA), a disorder marked by partial
collapse of the pharynx during inspiration, resulting in loud
snoring and gasping for air.13
Loose lid and poor lid/globe congruity.
Symptoms generally consist of ocular injection, irritation, itching
and stringy mucous discharge, particularly upon awakening. The
symptoms may appear unilaterally or asymmetrically. Patients
with OSA may also complain of erratic sleep patterns, chronic
somnolence and morning headaches.
Examination of patients with FES typically reveals chronic
papillary conjunctivitis with mild to moderate bulbar hyperemia,
often lateralizing to the patient's habitual sleeping side (i.e., if
they sleep on their left side, the presentation is more evident O.
S.). Punctate corneal epitheliopathy and mucous strands in the
tear film and fornices may also be apparent. The lids themselves
routinely display pseudoptosis and an odd "rubbery" consistency.
Eversion of the upper lids can be accomplished with minimal
manipulation; in fact, it may occur spontaneously during normal
ocular examination. Past ocular history may include meibomian
gland dysfunction, hordeola or chalazia, keratoconus, and
Loose lid upon eversion.
seasonal allergic conjunctivitis.
Pathophysiology
The etiology of FES is not thoroughly understood. Research has demonstrated that tarsal elastin is
significantly diminished in these patients, such that the tarsal plate of the eyelid no longer displays its
customary rigidity.4 One study suggests that individuals with FES may actually have underlying
genetic collagen or elastin abnormalities.5
The precise mechanism of this disorder also remains disputed. The most widely held theory suggests
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Handbook of Ocular Disease Management - Floppy Eyelid Syndrome
that, because of the lid laxity and tendency of these patients to lie on their sides or in a "face-down"
position, spontaneous lid eversion occurs during sleep. This results in mechanical abrasion of the
ocular surface. Others have suggested that the underlying mechanism is simply poor apposition of
the upper eyelid to the globe, instigating an inadequate tear distribution and subsequent desiccation
of the ocular surface.
Management
In the majority of cases, diagnosis is made by the classic appearance and effortless or spontaneous
eversion of the eyelids. There are few ancillary tests to consider beyond the normal ocular evaluation,
though vital dye staining (e.g., sodium fluorescein, rose bengal and/or lissamine green) may help to
assess the severity of any associated keratopathy.
Treatment for FES consists primarily of lubricating the ocular surface and safeguarding the eye from
nocturnal damage. Isotonic artificial tears, used liberally throughout the day, help to eliminate mucous
debris and promote corneal healing. In cases of moderate or profound epitheliopathy, consider more
viscous lubricants such as Systane or Refresh Liquigel on a qid basis. At bedtime, the patient should
instill either a bland ophthalmic ointment (e.g. Tears Naturale P.M.) or mild antibiotic ointment and
apply a protective eye shield, or simply tape the lids in a closed position. Severe, recalcitrant cases
that do not respond to primary therapy may require surgical intervention. Most commonly, this
involves a lateral eyelid tightening procedure at the lateral canthus, or a horizontal lid shortening
procedure by full-thickness resection of the lateral one-third of the lid margin.6 Lateral tarsorrhaphy
has been suggested for noncompliant patients with severe disease.7
As important as managing the ocular sequelae of FES is addressing the associated problem of
obstructive sleep apnea. OSA is a potentially fatal condition that has been linked to pulmonary
hypertension, congestive heart failure and cardiac arrhythmia. Weight loss and consultation with a
sleep physician for appropriate studies are highly recommended, considering the significant
comorbidities of both obesity and OSA. At least one study has demonstrated notable improvement of
FES when OSA is properly addressed.8
Clinical Pearls
●
Many patients with FES manifest attendant blepharitis, particularly meibomian gland
dysfunction. Rosacea has also been found in association with both FES and OSA. Strongly
consider a trial of oral doxycycline 100mg bid for six to 12 weeks.
●
When interviewing patients with FES, always remember to inquire about prominent snoring or
gasping episodes during sleep. In this regard, realize that a spouse or family member may
actually prove to be a more reliable resource than the patient! Any such findings consistent
with OSA warrant consultation with a sleep physician, otolaryngologist or pulmonologist.
1. McNab AA. Floppy eyelid syndrome and obstructive sleep apnea. Ophthal Plast Reconstr Surg 1997;13
(2):98-114.
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Handbook of Ocular Disease Management - Floppy Eyelid Syndrome
2. Mojon DS, Goldblum D, Fleischhauer J, et al. Eyelid, conjunctival, and corneal findings in sleep apnea
syndrome. Ophthalmology 1999;106(6):1182-5.
3. Robert PY, Adenis JP, Tapie P, et al. Eyelid hyperlaxity and obstructive sleep apnea (O.S.A.) syndrome. Eur
J Ophthalmol 1997;7(3):211-5.
4. Netland PA, Sugrue SP, Albert DM, et al. Histopathologic features of the floppy eyelid syndrome.
Involvement of tarsal elastin. Ophthalmology 1994; 10(1)1:174-81.
5. Lee WJ, Kim JC, Shyn KH. Clinical evaluation of corneal diseases associated with floppy eyelid syndrome.
Kor J Ophthalmol 1996;10(2):116-21.
6. Periman LM, Sires BS. Floppy eyelid syndrome: A modified surgical technique. Ophthal Plast Reconstr Surg
2002;18(5):370-2.
7. Bouchard CS. Lateral tarsorrhaphy for a noncompliant patient with floppy eyelid syndrome. Am J
Ophthalmol 1992;114(3):367-9.
8. McNab AA. Reversal of floppy eyelid syndrome with treatment of obstructive sleep apnoea. Clin Experiment
Ophthalmol 2000;28(2):125-6.
Other reports in this section
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Floppy Eyelid Syndrome
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Handbook of Ocular Disease Management
DERMATOCHALASIS & BLEPHAROCHALASIS
Signs and Symptoms
Dermatochalasis describes a common, physiologic condition
seen clinically as sagging of the upper eyelids, and to some
degree, the lower lids. It is typically bilateral and most often seen
in patients over 50 years of age, but may infrequently occur in
some younger adults. Inspection of these patients' lids reveals
redundant, lax skin with poor adhesion to the underlying muscle
and connective tissue. An excess flap or fold of skin in the upper
lid is characteristic, and the normal upper lid crease may be lost.
Dermatochalasis typically results in a ptosis, though occasionally
patients will utilize the frontalis muscle to pull the lids open; this
eliminates the ptosis but results in a wrinkling or furrowing of the
forehead. Additional findings may include upper eyelid entropion, Upper eyelid swelling in
lower eyelid ectropion, blepharitis, or dermatitis.
blepharochalasis.
Most commonly, dermatochalasis presents a cosmetic concern only, with patients complaining of
"droopy eyelids" and "bags under the eyes," which may cause them to appear "older than they truly
are." Some patients report true functional difficulties however, the most common being obstruction of
the superior visual field.1 Less commonly, patients may complain of ocular irritation secondary to
misdirected lashes or chronic blepharitis.
Dermatochalasis is sometimes confused with blepharochalasis. Though similar in nomenclature,
these two disorders are quite different in presentation and etiology. Blepharochalasis is a rare
condition that appears to be inflammatory in nature. It typically affects only the upper eyelids, and
may be unilateral as well as bilateral.2 It is encountered more commonly in younger rather than older
individuals.3 The condition is characterized by exacerbations and remissions of eyelid edema, which
results in a "stretching" and subsequent atrophy of the eyelid tissue. Complications of
blepharochalasis may include conjunctival hyperemia and chemosis, entropion, ectropion, and ptosis.
Pathophysiology
The tissue alterations encountered in dermatochalasis are not unlike the normal aging changes of the
skin seen elsewhere in the body. There is thinning of the epidermal tissue with a loss of elastin,
resulting in laxity, redundancy, and hypertrophy of the skin. The etiology of dermatochalasis appears
to be nothing more than repeated facial expression--smiling, laughing, squinting, crying, etc.--
combined with the action of gravity over many years. Less commonly, systemic disorders such as
Ehlers-Danlos syndrome, cutis laxa, thyroid eye disease, renal failure, and amyloidosis may hasten
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Handbook of Ocular Disease Management
the development of dermatochalasis.4 Some patients may additionally have a genetic predisposition
toward developing dermatochalasis at a younger age.
Blepharochalasis stems from recurrent bouts of painless eyelid swelling, each instance of which may
persist for several days. The swelling most likely represents a form of localized angioedema, although
this remains speculative. Ultimately, after numerous episodes, the skin of the lids becomes thin and
atrophic, and damage to the levator aponeurosis ensues. Ptosis then becomes manifest.
Blepharochalasis is idiopathic in most cases, though it has been linked to kidney agenesis, vertebral
abnormalities, and congenital heart defects in rare instances.5
Management
Patients with asymptomatic dermatochalasis require little
trea tment, although automated perimetry may be
beneficial to document any significant compromise to the
visual field and is often necessary prior to surgical
correction. Patients should also be evaluated for
blepharitis, trichiasis, or dry eye and treated accordingly
with palliative and/or therapeutic agents. If examination
reveals any other indications of underlying systemic
disorders (e.g. thyroid or renal disease), then
appropriate laboratory testing should be performed.
Those individuals with symptomatic dermatochalasis
should be referred for oculoplastic consultation with
regard to blepharoplasty, which is the procedure of
Dermatochalasis.
choice for this condition. Patients with significant ptosis
due to levator dehiscence may require a combined procedure.
Likewise, blepharoplasty with or without ptosis repair is the preferred management option for patients
with symptomatic bleph-arochalasis.6 Acute instances of lid swelling may be addressed with cold
compresses and oral anti-inflammatory agents in hopes of averting the ultimate outcome.
Clinical Pearls
●
Realize that dermatochalasis is a normal, physiologic condition that affects virtually all patients
over the age of 50, to varying degrees. It is commonly asymptomatic and requires little
intervention. In contradistinction, blepharochalasis is an atypical, pathologic syndrome that can
result in significant visual impairment of young, active adults.
●
A common feature to both dermatochalasis and blepharochalasis is the herniation of orbital fat
through the septum orbitale in the upper or lower eyelids. This phenomenon is referred to as
steatoblepharon. Like dermatochalasis, steatoblepharon is common with age, and may be
quite pronounced in some individuals. It is most often noted in the medial upper eyelid.
Treatment of this condition involves transconjunctival blepharoplasty with resection of the
excess fatty tissue.
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Dermatochalasis should not be confused with floppy eyelid syndrome, a condition in which the
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Handbook of Ocular Disease Management
lids become flaccid due to a loss of tarsal elastin.
1. Fay A, Lee LC, Pasquale LR. Dermatochalasis causing apparent bitemporal hemianopsia. Ophthal Plast
Reconstr Surg 2003;19(2):151-3.
2. Collin JR. Blepharochalasis. A review of 30 cases. Ophthal Plast Reconstr Surg 1991; 7(3):153-7.
3. Huemer GM, Schoeller T, Wechselberger G, et al. Unilateral blepharochalasis. Br J Plast Surg 2003; 56
(3):293-5.
4. DeAngelis DD, Carter SR, Seiff SR. Dermato-chalasis. Int Ophthalmol Clin 2002; 42(2):89-101.
5. Ghose S, Kalra BR, Dayal Y. Blepharochalasis with multiple system involvement. Br J Ophthalmol 1984; 68
(8):529-32.
6. Custer PL, Tenzel RR, Kowalczyk AP. Blepharochalasis syndrome. Am J Ophthalmol 1985; 99(4):424-8.
Other reports in this section
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Handbook of Ocular Disease Management
DACRYOCYSTITIS
Signs and Symptoms
The nasolacrimal apparatus drains the tears and tear constituents from the lacrimal lakes of the eyes into the nose.1-8 Pain, redness
and swelling over the inner aspect of the lower eyelid and epiphora may signify aggravated blepharitis, meibomianitis or canaliculitis. If
the problem becomes recurrent, associated with fever and severe erythematous swelling around the nasal aspect of the lower lid
involving the lacrimal sac such that a mucopurulent discharge can be expressed from the inferior punctum when pressure is applied,
the suspicion of dacryocystitis should be high.26,8
Pathophysiology
Swollen nasolacrimal system in
dacryocystitis.
The system consists of inferior and superior puncta (which lie in the nasal canthi of both eyes), their attached 10mm canaliculi (each of
which possess a 2mm vertical segment), and an 8mm nasal running segment, which courses 10mm through the lacrimal sac to the
common 17mm interosseous/intermembraneous nasal lacrimal duct that drains into the nose through the valve of Hasner beneath the inferior turbinate.4,6
The primary etiology of dacryo-cystitis is nasolacrimal apparatus obstruction secondary to mucocele of the lacrimal sac which is precipitated by chronic blockage of the interosseous
or intermembraneous nasolacrimal duct.4,6 Most cases of nasolacrimal duct obstruction are found in the older population, resulting from chronic mucosal degeneration, ductile
stenosis, stagnation of tears and bacterial overgrowth.3,4,8 Infantile dacryocystitis is uncommon but presents with the same signs and symptoms. A study examining the most
frequently recovered anaerobes from dacryo-cystitis reported Pepto-streptococcus spp., Propionibacterium spp., Prevotella spp. and Fusobacterium spp. as the most frequently
associated pathogens.8
Lacrimal sac obstructions often produce signs and symptoms that are similar to dacryocystitis but not as severe. They are collectively known as canaliculitis. These infections are
differentiated by solid concretions called dacryoliths, which can be found and expressed from the infected lacrimal sac.
Dacryoliths are caused by the bacteria Actinomyces israelii (Streptothrix), fungi such as Candida, Aspergillus or Fusarium, and viruses such as herpes simplex virus and varicella
virus. When present, dacryoliths should be removed with curettage or canaliculotomy, cultured and treated accordingly with both topical and oral antibiotic, antiviral or antifungal
preparations.2-4
Management
Management of the nonfebrile child includes oral amoxicillin/clavulanate (Augmentin, GlaxoSmithKline) 2040mg/kg/day, po, tid or oral cefaclor 2040mgs/ kg/day po, tid, along with
topical antibiotic drops qid, ointments bid, warm compresses and acetaminophen. Management of the adult nonfebrile patient includes cephalexin (Keflex, Lilly) or Augmentin 500mg
po, qid along with topical antibiotic drops, ointments, warm compresses and aspirin or ibuprofen for pain and inflammation, as needed.
Management of the febrile patient must be handled with extreme caution.
Patients who are acutely ill should be hospitalized and placed on IV cefazolin (Ancef, Glaxo-SmithKline) q8h along with the other modalities. CT or MRI should be considered when
other etiologies or differentials are in question.
In a recent study, polyurethane stents placed into the cannilicular apparatus were evaluated as a percutaneous management of the persistent epiphora left by canilicular disease.7
Minor postoperative complications such as epistaxis, palpebral edema, headache and, ironically, two acute cases of dacryocystitis were recorded. The initial technical success rate
of stent placement was 95%. The average time of the procedure was six minutes. Resolution of epiphora was complete in 452 eyes and partial in 18. On follow-up, 340 of 496 stents
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remained patent. Of the 156 obstructed stents, 114 were withdrawn and 49 of these patients remained asymptomatic for a mean of 27 months. After stent removal, the sac
configuration was unchanged in 81.5%, contracted in 9.6%, and widened in 8.8% of cases. The procedure appears to be simple and safe, both in stent insertion and in withdrawal.
The success rate was >75% in the short term and >55% in the long term. While not totally without concerns, the technique is attractive for most patients who prefer not to undergo
surgery or are unsuitable surgical candidates.7
An even more recent study set out to investigate whether acute dacryocystitis complicated by abscess formation could be successfully treated using laser-assisted endonasal
dacryocystorhinostomy (DCR).6 Resolution of symptoms and signs of acute dacryocystitis occurred in all nine patients treated.6 No recurrence of acute dacryocystitis occurred
during the median follow-up period of 11 months.6 Laser assisted endonasal DCR appears to be an effective tool in the primary treatment of acute dacryocystitis complicated by
abscess formation.6 In addition, any pre-existing symptoms of epi-phora or recurrent nasolacrimal infections seem to be concurrently relieved following the procedure in the majority
of patients.6
Clinical Pearls
●
Obstruction of the tear drain-age system can occur at any age.
●
Punctal stenosis may result from conjunctival diseases such as Stevens-Johnson syndrome (dry eye, dry mouth secondary to reaction to sulfa medicine), ocular cicatricial
pemphigoid, mechanical, thermal or chemical injury. In the young, congenital anomalies of the nasolacrimal system include congenital dacryostenosis, congenital
dacryocystocele and congenital canalicular fistula.26
●
Obstruction in the adult may result from midfacial trauma, sinus surgery, sinus infection or tumor. Bloody tears with a history of medial canthal mass should heighten
suspicion for space-occupying lesions. Facial cellulitis and acute ethmoidal or frontal sinusitis are among the important differential diagnoses.2,3,6
●
Prompt, decisive, aggressive management is essential.28 Hospital- ization with intravenous antibiotics should be considered in severe, febrile or recalcitrant presentations.
●
Punctal dilation and nasolacrimal irrigation is always contra-indicated in the acute stages due to risk of inducing preseptal cellulitis.
1. Weber AL, Rodriguez-De Valasquez A, Lucarelli MJ, et al. Normal anatomy and lesions of the lacrimal sac and duct: Evaluated by dacrtocyctography, computed tomography and mr imaging.
Neuroimaging Clinics of North America 1996;6(1):199-217.
2. Cullom RD, Chang B. Eyelid:Dacryocystitis; Inflammation of The Lacrimal Sac. In: Cullom RD, Chang B. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye
Disease. Philadelphia, PA; J.B. Lippincott Co. 1994:141-143.
3. Flanagan JC, Mazzoli RA. Oculoplastics. In: Tasman W., Jaeger EA. The Wills Eye Atlas of Clinical Ophthalmology. Philadelphia, PA; J.B. Lippincott Co. 1996:315-385.
4. Grove AS. Eyelids and Lacrimal System. In: Pavan-Langston D. Manual of Ocular Diagnosis and Therapy, 3rd ed. Boston, MA; Little, Brown and Co, 1991:47-55.
5. Weinstock FJ, Weinstock MB. Common eye disorders: six patients to treat, pitfalls to avoid. Postgraduate Medicine 1996;99(4):119-123.
6. Morgan S, Austin M, Whittet H. The treatment of acute dacryocystitis using laser assisted endonasal dacryocystorhinostomy. Br J Ophthalmol 2004;88(1):139-41.
7. Lanciego C, Toledano N, De Miguel S, et al. Resolution of epiphora with nasolacrimal stents: results of long-term follow-up in a multicenter prospective study. J Vasc Interv Radiol 2003;14
(11):1417-25.
8. Brook, I. Ocular infections due to anaerobic bacteria. Int Ophthalmol 2001;24(5):269-77.
Other reports in this section
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Dacryocystitis
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HERPES SIMPLEX BLEPHARITIS
Signs and Symptoms
Herpes simplex virus (HSV) blepharitis is encountered primarily in children, although adults may also
manifest this disorder. Presenting symptoms include variable pain and tenderness upon palpation, as
well as increased lacrimation in severe cases. If the conjunctiva is involved, tarsal follicles may be
observed along with bulbar injection and chemosis. A swollen pre-auricular node on the involved side
is common.
HSV infections involving the lid may present in one of
two forms. The classic appearance involves an
accumulation of small vesicles or pustules along the lid
margin and/or periocular skin. These lesions typically
have an inflamed, erythematous base. Within the first
week of infection, the vesicles may ulcerate or harden
into crusts, although they will ultimately resolve without
scarring.
A second "erosive-ulcerative" form of HSV blepharitis
has also been described.1 This presentation is
characterized by erosions of the lid at the gray line or
Pustular herpes simplex blepharitis
ulcers along the lid margin, or a combination of both.
The lid typically displays generalized swelling and redness associated with these lesions. The lesions
usually number no more than three and, like the classic variety, they generally resolve without scar
formation.
Pathophysiology
Herpes simplex is the most common virus found in humans. A member of the Herpetoviridae family,
HSV is a double-stranded DNA virus that replicates within cell nuclei. As it leaves the host cell, it
becomes encapsulated and can lie dormant for extended periods of time. Several trigger factors,
including fever, trauma, emotional stress, menstruation, exogenous immunosuppressive agents, and
overexposure to UV radiation can activate the virus. Transmission typically occurs by direct contact
with open epithelial lesions or contaminated bodily secretions. Rarely, contaminated materials, such
as towels or tissues spread the virus.
Primary ocular infections occur most often in children between the ages of six months and five years,
and almost invariably present as blepharitis or blepharoconjunctivitis. In recurrent attacks, the virus
usually reappears as a dendritic keratitis. Several reports of recurrent HSV blepharitis have been
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reported in the literature, however.2,3
Management
There is no specific treatment for HSV blepharitis, and most often
the course of the disease is self-limiting within two to three
weeks.4 The use of warm saline compresses with a topical drying
agent (e.g., 70% alcohol or aluminum sulfate [Domeboro, Bayer]
solution) is usually sufficient to palliate the patient. If the lesions
are extensive, concomitant use of topical antibiotic ointment is
considered prudent to prevent a secondary bacterial infection.
The use of topical or oral antiviral agents has not been proven to
enhance the recovery of patients with HSV blepharitis, although
the use of antivirals is still advocated by some practitioners for
more severe cases. Topical trifluridine 1% (Viroptic, Monarch) is
Erosive/ulcerative herpes simplex
absolutely indicated, however, in cases presenting with corneal
blepharitis.
involvement. The use of topical steroids on HSV lid lesions may
be un-wise, particularly if there is other ocular involvement. Although corticosteroids may be used
without fear in cases of herpes zoster (HZO) blepharitis, their use in cases of HSV infection may
predispose the patient to the eruption of a dendritic keratitis.
Clinical Pearls
●
The differential diagnosis of HSV blepharitis should always include HZO. Keep in mind,
however, that HZO typically affects elderly patients over the age of 70. Younger patients who
present with HZO are often immunocompromised secondary to disorders such as AIDS or
lymphoma. HSV blepharitis is usually encountered in children, but can occur at any age.
●
Although herpes simplex is known as a sexually transmitted disease, the vast majority of
ocular herpes infections are not contracted via sexual contact. This is important to recognize
when considering pediatric cases of HSV blepharitis.
●
While the acute management of HSV blepharitis does not seem to require or benefit greatly
from oral antiviral agents, the Herpetic Eye Disease Study showed that the recurrence of
herpes simplex virus eye disease is decreased when long-term acyclovir is used.5 Thus,
patients who experience two or more recurrences of HSV blepharitis should be offered the
option of prophylactic therapy consisting of oral acyclovir 400mg bid.
1. Egerer I, Stary A. Erosive-ulcerative herpes simplex blepharitis. Arch Ophthalmol 1980; 98(10):1760-3.
2. Besada E. Clinical diagnosis of recurrent herpes simplex blepharitis in an adult: A case report. J Am Optom
Assoc 1994;65(4):235-8.
3. Kabat AG, Espejo A, Canavan K, et al. Recurrent herpes simplex blepharoconjunctivitis following HSV
keratitis in an adult. Optom Vis Sci 1998; 75(12s):120.
4. Lee SY, Laibson PR. Medical management of herpes simplex ocular infections. Int Ophthalmol Clin 1996;36
(2):85-97.
5. The Herpetic Eye Disease Study Group. Acyclovir for the prevention of recurrent herpes simplex virus eye
disease. N Engl J Med 1998; 339(5):300-6.
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Other reports in this section
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XANTHELASMA
Signs and Symptoms
Xanthelasma are seen clinically as oval or elongated yellowish
plaques just beneath the skin of the periorbital region. Most
commonly, they are noted near the inner canthus of the upper
eyelid, although they may be seen on the lower lid as well; they
are generally symmetrical in presentation. Inspection and
palpation may reveal a soft, semisolid, or calcified texture.
Patients with xanthelasma are typically over 40 years of age, and
women are affected nearly twice as often as men.1 The condition
may be seen in light-skinned and dark-skinned individuals.
Patients with xanthelasma may present because of a cosmetic
concern, or the condition may be detected on routine ocular
Placoid xanthelasma lesion.
examination. The lesions are neither inflammatory nor painful,
(Courtesy Drs. Julie Tyler and
Alexandra Espejo)
and there is no tendency toward malignancy, although the lesions
may enlarge and/or coalesce over time. In very rare instances, abnormally large xanthelasmas can
interfere with lid function, causing ptosis or lagophthalmos.
Pathophysiology
Xanthelasma palpebrarum represents a common form of xanthoma, a cutaneous deposit of fatty
materials. The term "xanthelasma" is extremely descriptive; it is derived from the Greek xanthos
(meaning yellow) and elasma (meaning plate). Histological evaluation of these lesions reveals an
accumulation of lipid-laden macrophages, termed histiocytes, within the dermis.
Although a link has been suggested between xanthelasma and hyperlipidemia, only about half of
patients with these lesions demonstrate elevated serum lipid levels. However, younger individuals
with xanthelasma have a proportionally greater likelihood of hyperlipidemia and hypercholesterolemia
than do older individuals.2,3
Management
In most cases, xanthelasma is diagnosed by the clinical appearance alone, though atypical
presentations may prompt the clinician to obtain a biopsy. Laboratory testing of serum lipids is also
recommended.
While xanthelasma is essentially benign, many patients consider the condition to be cosmetically
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unacceptable, and opt for removal. Treatment modalities are quite numerous, and include such
diverse options as: (1) use of chemocautery agents, such as trichloracetic acid; (2) electrodessication;
(3) cryotherapy; (4) CO2 or argon laser ablation; or (5) surgical excision. Scar formation and
pigmentary changes are the most common complications of laser or chemotherapy. Chemical cautery
and surgical excision tend to produce better results with less risk of subsequent scarring.
Clinical Pearls
●
While we know that xanthelasma may be an indication of abnormal lipid levels, it is equally
important to realize that other metabolic disorders can lead to increased serum lipids,
particularly diabetes and cirrhosis of the liver.4 There-fore, appropriate testing includes not only
a serum lipid profile, but also a fasting plasma glucose and liver function tests (both of which
are part of a comprehensive metabolic panel, or CMP, the single most common blood panel
ordered by physicians).
●
Patients should be aware that, despite effective local treatment for xanthelasma, recurrences
can and often do occur.
●
Although dietary modification and medications to reduce hyperlipidemia may be beneficial for
other co-morbidities, there is no evidence that this form of therapy has any impact on the
appearance or resolution of xanthelasma.5
1. Gladstone GJ, Myint S. Xanthelasma. In: Fraunfelder FT, Roy FH, eds. Current Ocular Therapy, 5th Edition.
Philadelphia: W.B. Saunders, 2000. 452-3.
2. Ribera M, Pinto X, Argimon JM, et al. Lipid metabolism and apolipoprotein E phenotypes in patients with
xanthelasma. Am J Med 1995; 99(5):485-90.
3. Bergman R. Xanthelasma palpebrarum and risk of atherosclerosis. Int J Dermatol 1998; 37(5):343-5.
4. Premalatha G, Mohan V. Xanthelasma palpebrum a marker for hyperlipidemia in NIDDM patients? J Assoc
Physicians India 1996; 44(1):73-4.
5. Dean FD. Xanthelasma and hyperlipoproteinaemia. Clinica Chimica Acta 1976; 66(2):189-93.
Other reports in this section
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Handbook of Ocular Disease Management - Understanding Corneal Topography
Understanding Corneal Topography
Within the past 10 years, corneal topography
has grown from an elaborate and costly device
used only for clinical research in large
institutions to a critical in-office tool that many
optometrists now use daily. Along with
advances in computerization and software
development, topographers have become
fig01.jpg (5755 bytes)
smaller, more compact, more affordable and
more precise. This primer describes the
mechanics, methods of interpreting the data,
and indications for performing corneal
topography.
The Mechanics Behind Topography
Some topography units create both elevation and
Corneal topography--also known as
axial maps, and provide statistical indices. (Courtesy
videokeratography or corneal mapping--
Ken Lebow, O.D.)
represents a significant advance in the
measurement of corneal curvature over keratometry. Most corneal topographers evaluate 8,000 to
10,000 specific points across the entire corneal surface. By contrast, keratometers measure only four
data points within the cornea's central 3-4mm; the small size of this area can lead to errors in
determining precise toricity.
Topography provides both a qualitative and quantitative evaluation of corneal curvature. It does so by
utilizing concentric rings, which project onto the cornea to create a virtual image. The device
compares this image to the target size, and the computer then calculates the corneal curvature.
Although many different systems are available, all share some unifying measurement characteristics.
The computer ized topographer can generate various graphical representations. When performing
corneal mapping for diagnosis of conditions and/or contact lens fitting, the two most common maps
that practitioners use are:
• Axial map. Also called the "power" or "sagittal" map, this output is the simplest of all the
topographical displays. It shows variations in corneal curvature as projections and uses colors to
represent dioptric values. Warm colors such as red and orange show steeper areas; cool colors such
as blue and green denote the flatter areas.
The axial map gives a global view of the corneal
curvature as a whole. Its downside is its
tendency to ignore minor variations in
curvature.
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• Tangential map. Sometimes referred to as
the instantaneous, local, or "true" map, it also
displays the cornea as a topographical
illustration, using colors to represent changes in
dioptric value. However, the tangential strategy
bases its calculations on a different
fig01.jpg (5755 bytes)
mathematical approach that can more
accurately determine the peripheral corneal
configuration. It does not assume the eye is
spherical, and does not have as many
presumptions as the axial map regarding
corneal shape. In fact it is the map that more
closely represents the actual curvature of the
cornea over the axial map. The tangential map
This elevation map shows inferior thinning in a
recognizes sharp power transitions more easily
patient's left eye. (Courtesy Ken Lebow, O.D.)
than the axial map, and eliminates the
"smoothing" appearance that appears on the axial map. This is not universally true for all
topographers.
Compared with axial maps, tangential maps yield smaller patterns with details that are more centrally
located. Tangential maps also offer a better visualization of the precise location of corneal defects.
This display is most useful in following trends in the postsurgical or pathologic eye.
There are two other types of corneal topography printouts clinicians use:
• Elevation map. This utilizes yet another algorithm to give additional information about the cornea.
An elevation map shows the measured height from which the corneal curvature varies (above or
below) from a computer-generated reference surface. Warm colors depict points that are higher than
the reference surface; cool colors designate lower points.
This map is most useful in predicting fluorescein
patterns with rigid lenses. Higher elevations
(reds) represent potential areas of lens bearing,
while the lower areas (greens) will likely show
fluorescein pooling.
• Refractive map. This utilizes the measured
fig01.jpg (5755 bytes)
dioptric power and applies Snell's law to
describe the cornea's actual refractive power. A
refractive map compensates for spherical
aberrations as well as the aspheric contour of
the cornea. The central portion of the refractive
map is most important. This area overlies the
pupil, so aberrations here almost invariably
impact visual performance.
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This keratoconus screening program from the Tomey
TMS-3 topographer provides two analysis methods.
Clinicians use refractive maps to evaluate visual
performance in post-refractive surgery patients. This view identifies central islands in patients who
have undergone PRK or LASIK.
Scaling is another important consideration with corneal topography. In most topographers, the user
can utilize the auto-size or normalized scale (relative scale). This strategy essentially subdivides the
cornea into dioptric intervals based on its actual curvature range (usually a 6.00D range). Recognize
that the actual colors are not specific to a dioptric value when using the normalized scale, but rather
are relative to that particular patient's eye.
By contrast, the absolute or standard scale assigns a specific color to each dioptric value and
constrains the data to fit within that range. This strategy allows you to directly compare images from
different eyes or from significant curvature changes in one eye (e.g., pre- vs. postoperative refractive
surgery status). The downside to using the standard scale is that the dioptric range is greatly
expanded; hence, clinically significant irregularities may become somewhat obscured when
comparing eyes with very different curvature readings. Clinically, it is probably best to use normalized
(relative) maps when evaluating one particular eye, and use standard maps when comparing two
different eyes or comparing the same eye over time.
Clinical Indications
Topography may be indicated in many clinical situations. Conditions such as keratoconus and
pellucid marginal degeneration may exhibit corneal steepening before any biomicroscopic signs are
evident. In keratoconus, the color maps provide information of the location, size and curvature of the
cone's apex, and can help you follow the progression of the disease.
Topography also is invaluable when evaluating pre- and postsurgical patients, particularly those who
have had penetrating keratoplasty, radial keratotomy or LASIK. Preoperatively, corneal maps give
insight into potential obstacles, such as scarring or irregular astigmatism. Postoperatively, topography
can help follow the healing phase and assist with contact lens fitting.
Finally, corneal topography may lend insight
into those unusual or difficult refractive cases.
Patients with high corneal cylinder often pose a
significant challenge when performing
retinoscopy and/or auto-refraction, as well as
standard keratometry. The topographer is just
one more tool that can help you obtain valuable
information in assessing refractive error.
The most profitable and practical use of corneal
topography in clinical practice is seen in the
fitting of gas permeable lenses. Corneal
topography is also useful for annually
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evaluating the topographical impact of corneal
changes in soft contact lens patients. It is also
virtually mandatory in corneal reshaping
(Corneal Refractive Therapy or orthokeratology)
to monitor the corneal changes occurring as
well as the lens positioning from overnight wear.
Most corneal topographers provide software
fig01.jpg (5755 bytes)
that can design an appropriate contact lens
based upon the topography. They recommend
lens material, size, design, and even simulate a
fluorescein pattern. You can manually alter
diameter; base curve and edge design and
observe the impact on the simulated pattern.
There are even bitoric fitting programs designed
for highly astigmatic patients. This software can
greatly simplify the gas permeable fitting
The refractive module in the Dicon-Paradigm unit can
display pre- and post-op results, and track
process, reduce chair time and increase patient
keratometric powers over time.
satisfaction.
When considering contact lens correction for these corneal conditions, corneal topography is
practically mandatory:
• Post-penetrating keratoplasty, which often results in high or irregular corneal astigmatism;
• Post-RK or LASIK, in which the central cornea flattens relative to the periphery, potentially resulting
in residual refractive error and irregular astigmatism;
• Advanced keratoconus, in which the central and peripheral curves of the lens are critical to
accommodate the protruding cone.
The information corneal topography provides can greatly enhance your ability to manage complex
contact lens fits and increase your overall success rate. While many doctors were discouraged in
years past by the high cost of this equipment, the prices have decreased dramatically. Also, many
manufacturers now provide leasing packages that offset the initial investment costs.
Corneal mapping devices and contact lens fitting programs will continue to improve and expand their
capabilities in the future. Indeed, today it is arguably the standard of care for our profession.
The authors have no direct financial interest in any company that manufactures corneal topographers.
Other reports in this section
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Handbook of Ocular Disease Management - Corneal Abrasion and Recurrent Corneal Erosion
CORNEAL ABRASION AND RECURRENT CORNEAL EROSION
Corneal Abrasion
Recurrent Corneal Erosion
SIGNS AND SYMPTOMS
Symptoms of acute pain and a history of recent trauma are obviously the tell-tale indicators of a corneal
abrasion, but the patient may also report photophobia, pain upon extraocular muscle movement, excessive
tearing, blepharospasm, foreign body sensation and blurry vision. Slit lamp exam of the injured area may reveal
diffuse corneal edema and epithelial disruption. In severe cases, when edema is excessive, you may see folds in
Descemet’s membrane. With fluorescein staining, the newly created wound will appear as a bright green area
compared to the rest of the cornea as the dye accumulates in the divot.
Recurrent corneal erosion (RCE) is characterized by repeated, spontaneous disruption of the corneal
epithelium. In most cases, the malady is preceded by mechanical trauma, such as a corneal abrasion caused by
a fingernail.
Patients with RCE usually present to the office with a history of corneal abrasion in the involved eye, often
months or years previously, and a chief complaint of recurrent episodes of ocular pain that may also include
foreign body sensation, photophobia, blepharospasm, decreased vision or lacrimation upon awakening or
following eye rubbing or eye opening.
Clinical signs include a localized, visible roughening of the corneal epithelium which stains superficially with
fluorescein dye. The lesions are typically unilateral and in the vicinity of the original corneal defect. Bilateral
or idiopathic lesions suggest a basement membrane dystrophy. The phenomenon may occur as frequently as
daily or as sparsely as biweekly or monthly.
Epithelial basement dystrophy is an associated finding in many cases. It is marked by small, intra-epithelial
dots and subepithelial ridges and lines (“maps”, “fingerprints”), representing poor adhesion of the epithelial
basement membrane and Bowman’s layer.
PATHOPHYSIOLOGY
There are two categories of abrasions: superficial (those not involving Bowman’s membrane) and deep (those
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that penetrate Bowman’s membrane, but do not rupture Descemet’s membrane). Abrasions may result from
foreign bodies, contact lenses, chemicals, fingernails, hair brushes, tree branches, dust and the like.
The cornea has remarkable healing properties. The epithelium adjacent to any insult expands in size to fill in
the defect, usually within 24 to 48 hours. Lesions that are purely epithelial often heal quickly and completely
without scarring. Lesions that extend below Bowman’s are more likely to leave a permanent scar.
The epithelial healing process begins when basal epithelial cells undergo mitosis, producing new cells that
occupy fresh wounds. Basal cells adhere the epithelium to the stroma in two ways: they secrete the basement
membrane and they contain hemidesmosomes, which are essentially linchpins that protrude through the
posterior surface of basal cells and into the stroma; each is held in place by an anchoring fibril. Any disruption
to basal cell production will make the eye more prone to recurrent erosion.
MANAGEMENT
For a corneal abrasion, first evert the eyelid and scrutinize the palpebral conjunctiva, ocular surface and
fornices to rule out the presence of foreign material. Instill fluorescein dye to identify the corneal defects. Next,
use the Seidel test (painting the wound with dye and observing for aqueous leakage) to uncover possible full-
thickness injuries. Document the size, shape, location and depth of the abrasion. Finally, evaluate the anterior
chamber and perform a dilated fundus exam to check for other effects of the trauma.
Begin treatment with cycloplegia (atropine 1% for the worst cases, homatropine 5% for moderate cases and
cyclopentolate 1% for the mildest) and a topical antibiotic such as Polytrim, gentamicin or tobramycin
(Tobrex). Recommend bed-rest, inactivity and OTC analgesics. If pain is severe, prescribe a topical
nonsteroidal anti-inflammatory (Voltaren, Acular or Ocufen, b.i.d. to q.i.d.) and/or a thin, low-water content
bandage contact lens.
Today, pressure patching is somewhat controversial. When patients are not in a great deal of discomfort, most
abrasions do not require patching. Larger abrasions may fare better with patching. The medicinal and
homeostatic effects of patching help to keep patients still, quiet and more comfortable. Reevaluate the patient
every 24 hours until the abrasion is re-epithelialized. Bandage soft contact lenses have nearly supplanted the
traditional pressure patch in the management of corneal abrasions.
Treat recurrent erosions in much the same way. But bear in mind that, in this instance, larger defects may
require patching. If pressure patching is unnecessary or contraindicated, prescribe a topical antibiotic drop q.i.d.
with an antibiotic ointment at bed-time.
If the corneal epithelium is not healing properly within 24 to 48 hours, debride the area to give the epithelium a
“clean slate” on which to regenerate. Instill a topical anesthetic, then remove the involved epithelium with a
cotton-tipped applicator soaked in saline. Any of the above steps can be followed after the procedure.
The most severe, recalcitrant cases may require anterior stromal puncture (purposeful scarring of the involved
area using a 23- to 25-gauge bent needle). This is accomplished by anesthetizing the cornea, then using the
needle to puncture the epithelium to the levels of Bowman’s membrane or anterior stroma in the affected area.
The final step in managing RCE is hypertonic therapy. Sodium chloride drops and ointments (2% and 5%)
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Handbook of Ocular Disease Management - Corneal Abrasion and Recurrent Corneal Erosion
applied to the eye q.i.d./q3h during the day and at bedtime will help to reduce corneal swelling, lubricate the
corneal surface and promote epithelial adherence. Interestingly, they also may help to restore vision.
CLINICAL PEARLS
●
For both medical and legal purposes, it’s important to take and record a detailed case history before
performing any procedures or treatments. Record the time, place and activity surrounding the injury, as
well as the presenting visual acuities.
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If the blepharospasm is sufficiently intense to preclude acuity testing, administer one drop of anesthetic
and try again.
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To promote healing, prevent recurrent erosion and reduce corneal edema, Rx a hypertonic solution or
ointment along with the other medications after re-epithelialization. If excess epithelium impairs
regrowth, use a cotton-tipped applicator saturated with anesthetic to debride loose tissue.
●
When there’s significant iritis present, Rx a steroid. Infiltrates may be a sign of infection or impending
ulceration. Consider such presentations to be vision threatening, and treat immediately with a
fluoroquinolone; also consider culturing the lesion.
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Patients with recurrent erosion require constant monitoring. Frequent use of use of thick artificial tear
drops and ointments will provide prophylactic lubrication and comfort. Bandage contact lens therapy is
another good treatment option. Thin, low-water content, disposable lenses provide reasonable drug
delivery while reducing the mechanical shearing forces on non-ulcerative, corneal epithelial lesions.
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Collagen punctal plugs may help identify individuals who would benefit from punctal occlusion or
punctal cautery.
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In cases of recalcitrant recurrent erosion, particularly those with vision-reducing corneal scars, consider
phototherapeutic keratectomy using an excimer laser, as well as diamond burr debridement and anterior
stromal puncture.
Other reports in this section
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Handbook of Ocular Disease Management - Corneal Foreign Body
Corneal Foreign Body
SIGNS AND SYMPTOMS
Patients who experience a foreign body of the cornea
generally present with mild, moderate, or occasionally
severe pain. Sometimes, the discomfort is described as a
scratchiness or the aptly named “foreign-body sensation.”
Excessive tearing, blurred vision and photophobia are also
common complaints. Upon inspection, the involved eye
may demonstrate lid edema, focal or circumlimbal
conjunctival injection, and a mild to moderate anterior
chamber reaction. The most critical sign is the finding of particulate matter at the surface of or
embedded within the cornea. If the foreign body is metallic, you’ll often see a rust ring surrounding
the object. If the foreign object remained embedded in the cornea for 24 hours or more, you may see a
ring infiltrate surrounding the site.
PATHOPHYSIOLOGY
Corneal foreign bodies generally fall under the category of minor ocular trauma. Small particles may
become lodged in the corneal epithelium or stroma, particularly when projected toward the eye with
considerable force. The foreign object sets off an inflammatory cascade, resulting in dilation of the
surrounding vessels and subsequent edema of the lids, conjunctiva and cornea. White blood cells are
also liberated, resulting in an anterior chamber reaction and corneal infiltration. A foreign body, if not
removed, can cause infection and/or tissue necrosis.
MANAGEMENT
Initially, it is important to ensure that the object has not perforated the cornea. If this is not possible
simply with slit lamp inspection, you must instill fluorescein to inspect for aqueous leakage through
the wound (Seidel’s sign). If there’s no penetration, remove the object under topical anesthesia (1-2
gtt 0.5% proparacaine). A direct stream of sterile irrigating solution may be sufficient to dislodge
some small foreign bodies. If this is not successful, use a flexible-loop foreign body spud or 25-gauge
needle to remove the object under the slit lamp.
CLINICAL PEARLS
●
When a corneal foreign body encroaches the visual axis, before proceeding, counsel patients
as to the potential loss of acuity due to unavoidable scarring; this conversation should be well
documented to avoid negative clinico-legal ramifications.
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If you are unable to rule out the possibility of a penetrating ocular injury, apply a shield to the
eye and refer the patient immediately to a nearby hospital or ophthalmology practice.
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Handbook of Ocular Disease Management - Corneal Foreign Body
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Handbook of Ocular Corneal Laceration
CORNEAL LACERATION
Signs and Symptoms
The patient with a corneal laceration has experienced significant
ocular trauma, typically from a metallic object such as a hand tool.
25aa.jpg (16690 bytes)
(Fingernail scratches, for example, do not usually have enough force
to lacerate a cornea.) There is intense pain initially which may
diminish slightly due to corneal desensitization. Patients are
photophobic and lacrimate profusely. There is a significant attendant
uveitis and the anterior chamber is shallow or even flat in a full
thickness laceration. Intraocular pressure generally ranges from 2 to
6 mmHg. Bubbles within the anterior chamber are a key finding.
There is significantly reduced visual acuity. Other associated
findings may include lens dislocation, iridodialysis, and hyphema.
25ab.jpg (8756 bytes)
Pathophysiology
A corneal laceration results from direct trauma to the cornea,
typically from a metallic object impacting with sufficient force.
There may be either a full thickness laceration or a partial thickness
laceration. A full thickness laceration is termed a penetrating injury.
In full thickness lacerations, there will be a flat chamber. Seidel’s
sign will be present: as fluorescein is added, you will see the
aqueous oozing out from the wound amidst the fluorescein. There
may also be bubbles in the anterior chamber. Damage to the iris may
25ac.jpg (17054 bytes)
result in an irregularly shaped, unreactive iris. Additional pressure
on the globe may result in extrusion of uveal tissue through the
wound.
Management
The diagnosis of corneal laceration must be made as quickly as
possible with as little intervention as possible. Additionally, a partial thickness laceration must be differentiated
from a full thickness laceration with the use of Seidel’s test. Intraocular pressure measurement should be
avoided in any cases suspected to be full thickness lacerations, as any pressure applied to the globe may cause
uveal tissue to extrude through the wound. Visual acuity must be taken, if possible. Judicious use of a topical
anesthetic will alleviate patient discomfort and allow the clinician to make an appropriate diagnosis. Open a
fresh bottle to avoid intraocular contamination.
Do not unnecessarily manipulate the eye with a full thickness laceration. A topical antibiotic solution may be
judiciously applied. Absolutely avoid pressure patch or bandage contact lens. Use an eye shield to protect the
eye. Again, exert no pressure upon the eye. Arrange for the corneal laceration to be surgically repaired by a
corneal specialist immediately. Instruct the patient to neither eat nor drink prior to the surgical consultation.
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Handbook of Ocular Corneal Laceration
Clinical Pearl
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With full thickness corneal lacerations, the less done in the office the better. Assess the injury, arrange
for the appropriate referral, and shield the eye gently for protection while the patient is in transit to the
surgeon.
●
With a corneal laceration, the patient frequently is lacrimating too heavily for the Seidel test to be
performed with any degree of accuracy. In these cases, a shallow or flat anterior chamber or the
presence of bubbles within the anterior chamber indicates a breach in the corneal integrity.
●
Advise the patient that the initial entering acuity may represent the best vision that the patient can
expect to achieve after surgical repair. Of course, vision may improve after surgical repair; however, it
is best not to elevate a patient’s expectations.
Other reports in this section
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Corneal Laceration
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Handbook of Ocular Disease Management - Sterile Corneal Infiltrates
Sterile Corneal Infiltrates
SIGNS AND SYMPTOMS
Unlike bacterial corneal ulcer patients, marginal sterile corneal ulcer
patients present with only mild conjunctival injection, little to no
conjunctival chemosis, ocular irritation and normal vision. One or
more marginal subepithelial corneal infiltrates are common in many
conditions, and usually do not warrant much concern. Accompanying
sequelae may include mild iritis, folds in Descemet's membrane if
there is substantial corneal edema, and posterior synechiae in chronic
cases.
Patients with Staphylococcal hypersensitivity reactions may present without symptoms. Here, scattered
multiple areas of sub-epithelial and anterior stromal infiltrates, with or without epithelial defects, line the
limbal area (mostly inferiorly). The entity is usually bilateral. One distinct characteristic is the notable clear
zone that lies between the areas of infiltrate and the limbus.
Frequently the patient will provide an ocular history of having a dry eye and a systemic history of rheumatoid
arthritis or other collagen vascular diseases. Other known associations are vernal keratitis, vitamin A-
deficiency and contact lens solution reaction. The principle differential diagnoses include infectious corneal
ulcer, marginal sub-epithelial infiltrates secondary to contact lens wear and Mooren's marginal corneal ulcer.
PATHOPHYSIOLOGY
Sterile infiltrates usually represent a low-grade immune response to bacterial exotoxins. For bacterial infection
or inflammation to occur, the microorganism must be able to adhere to the corneal surface. Staphylococcus
aureus, Streptococcus pneumoniae and Pseudomonas aeruginosa are significantly more adherent than other
organisms, possibly accounting for their more frequent involvement in corneal disease.. These organisms are
more adherent to the cornea and are tightly adherent to themselves, providing a resistance to phagocytosis by
host inflammatory cells.
Staph. aureus is recognized as one of the common opportunistic ocular pathogens. The organism is a gram-
positive non-encapsulated coccus capable of producing a variety of exotoxins and enzymes. In addition to its
ability to infect the central cornea, it is a leading cause of sterile marginal keratitis.
Powerful exotoxins released by bacteria colonizing the eyelid margin induce peripheral corneal destruction
through antigen-antibody reactions. Polymorphonuclear leukocytes and fibroblasts, which migrate to the area to
help fight exotoxins, produce collagenase and proteoglycanase enzymes that often produce additional damage.
MANAGEMENT
The treatment strategy for marginal sterile keratitis is two-fold: (1) control and eradicate the microorganism
and (2) control and eliminate the destructive elements and sequelae of inflammation. Eyelid scrubs BID/TID
using commercially available lid scrubs or baby shampoo will begin the process of cleansing the lid margins.
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Handbook of Ocular Disease Management - Sterile Corneal Infiltrates
To fully eradicate dense colonies of lid margin bacteria, prescribe a topical aminoglycoside (gentamicin,
tobramycin) or fluoroquinolone (ciprofloxacin, norfloxacin, ofloxacin) QID. The antibiotics kill the bacteria
and also mechanically wash organisms and their toxins away from the eyelid margin. If the patient complains
of discomfort, prescribe a cycloplegic. Rx a topical steroid based on the severity of the condition.
CLINICAL PEARLS
●
Since the corneal tissue is free from infection and its damage originates from the secondary effects of
inflammation, the most expeditious treatment is both topical antibiotics and topical anti-inflammatories.
Many practitioners are apprehensive about prescribing topical steroids in the face of corneal epithelial
compromise, although this does not usually pose a serious threat. Nevertheless, if you prefer a more
conservative approach, begin with antibiotic treatment alone for 24 to 48 hours, then judiciously add a
topical steroid thereafter and monitor for IOP rise.
●
Today, there is debate regarding the need to culture before starting treatment. Because culture results
are not available for 24 to 48 hours, many believe it is only necessary when a condition fails to respond
to the prescribed therapy. We advocate treating immediately and then culturing if the condition does not
improve or worsens within the first 48 to 72 hours.
Other reports in this section
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Handbook of Ocular Disease Management - Chemical Burns
Chemical Burns
SIGNS AND SYMPTOMS
The diagnosis of chemical trauma to the eye is typically based
upon the history, rather than the signs and symptoms. Patients
generally report varying degrees of pain, photophobia, reduced
vision, and colored haloes around lights.
In mild to moderate burns, the eye is hyperemic and may display conjunctival chemosis, eyelid edema,
first degree burns to the skin, and cells and flare in the anterior chamber. Corneal findings may range from
diffuse superficial punctate keratopathy to focal epithelial erosion with mild stromal haze.
When the chemical injury is severe, the eye is not red but appears white due to ischemia of the
conjunctival vessels. Chemosis of the lids and conjunctiva is evident, and surrounding facial areas may
demonstrate second or third degree burns. Corneal findings include total epithelial erosion with edema and
dense stromal hazing, and sometimes complete opacification.
PATHOPHYSIOLOGY
Both acidic (pH<4) and alkaline (pH>10) solutions are capable of inducing a chemical burn. Acids tend to
bind with tissue proteins and coagulate the surface epithelium. This bars further penetration so acid burns
are typically confined to superficial tissues. Most commonly, acid burns to the eye result from exploded
car batteries, which contain sulfuric acid.
Alkaline burns occur more frequently and are generally more severe than acid burns. These solutions
destroy the cell structure not only of the epithelium but also of the stroma and endothelium. While acids
create an initial burn and then cease, alkalis may continue to penetrate the cornea long after the initial
trauma. Common sources of alkalis include ammonia, lye and lime.
MANAGEMENT
A chemical burn requires immediate care. The patient needs prompt, copious fluid irrigation of the
affected eye, particularly with alkaline trauma. If the initial contact with the patient is by telephone, advise
flushing the eye with water for twenty to thirty minutes before coming to the office or clinic. If a patient
presents without having irrigated the eye, perform a prolonged lavage with saline solution before any other
procedures.
Next, test the eye with litmus paper to establish the residual pH. If near neutral (i.e. 6 to 8), the lavage may
be discontinued. Check the lids and fornices and remove any particulate matter (more common with drain
cleaners, cement, etc.). Debride any necrotic corneal or conjunctival tissue under the biomicroscope, using
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Handbook of Ocular Disease Management - Chemical Burns
a cotton-tipped applicator moistened with antibiotic solution; swab the fornices in a similar fashion.
Following this, a strong cycloplegic agent (e.g. 0.25% scopolamine) and broad spectrum antibiotic
ointment should be instilled.
If significant epithelial erosion has occurred, consider a pressure patch. In cases of very severe burns, the
patient may need to use a topical corticosteroid judiciously during the first week following trauma (1%
prednisolone acetate Q2-4H). Depending upon the level of pain, a narcotic analgesic may also be
necessary. Evaluate patients daily, and continue medications until resolved. It is also important to monitor
the intraocular pressure; IOP spikes may occur as late complications of chemical burns due to blockage of
the trabecular meshwork by inflammatory debris.
CLINICAL PEARLS
●
The most important consideration in chemical burns is immediate irrigation. This single measure
offers the best chance of reducing the ultimate physical damage to the eye.
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Know your "comfort zone." Don't hesitate to refer to a corneal specialist.
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Most acid burns are manageable if they present with mild to moderate stromal haze-they will only
get better with time. Alkaline burns, on the other hand, may require some thought, as the
presentation at day one may be far better than that seen at day two or three. If there is significant
necrosis and perilimbal ischemia at presentation, and if the cornea is even moderately hazy,
consider referring the patient as soon as the immediate condition is stabilize.
Other reports in this section
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Handbook of Ocular Disease Management - Chemical Burns
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Handbook of Ocular Disease Management - Bacterial Keratitis
Bacterial Keratitis
SIGNS AND SYMPTOMS
The patient will present with a unilateral, acutely painful,
photophobic, intensely injected eye. Visual acuity is usually reduced,
and profuse tearing is common. There will be a focal stromal
infiltrate with an overlying area of epithelial excavation. There is
likely to be thick, ropy, mucopurulent discharge.
The cornea will be very edematous. The conjunctival and episcleral vessels will be deeply engorged and
inflamed, often greatly out of proportion to the size of the corneal defect. In severe cases, there will be a
pronounced anterior chamber reaction, often with hypopyon. Intraocular pressure may be low due to secretory
hypotony of the ciliary body, but most often will be elevated due to blockage of the trabecular meshwork by
inflammatory cells. Often, the eyelids will also be edematous.
PATHOPHYSIOLOGY
Once the corneal defenses are breached, specifically the epithelial glycocalyx, the cornea is prone to infection.
Possible causes include direct corneal trauma, chronic eyelid disease, tear film abnormalities affecting the
ocular surface and hypoxic trauma from contact lens wear. Pathogenic bacteria colonize the corneal stroma and
immediately become antigenic, both directly and indirectly, by releasing enzymes and toxins.
This sets up an antigen-antibody immune reaction which leads to an inflammatory reaction. The body releases
polymorphonuclear leukocytes (PMNs) which aggregate at the area of infection, creating an infiltrate. The
PMNs phagocytize and digest the bacteria. The collagen stroma is poorly tolerant of the bacterial and
leukocytic enzymes and undergoes degradation, necrosis and thinning. This results in scarring of the cornea.
With severe thinning the cornea may perforate, creating the possibility for endophthalmitis.
Throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus
aureus. However, in cases involving contact lens wear and cosmetics, the most common infective organism is
Pseudomonas aeruginosa.
MANAGEMENT
As with bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting organism but
is often difficult or impractical. First and foremost, you must halt bacterial proliferation; do not delay treatment
while waiting for the culture results. If you have the materials available, scrape the ulcer using a platinum
spatula and plate the specimen onto blood and chocolate agar culture media. A simpler but less effective
method is to use a culturette.
Regardless, immediately begin therapy with a broad spectrum antibiotic. A popular initial therapy is the
fluoroquinolone ciprofloxacin 0.3% (Ciloxan) two drops every 15 minutes for six hours, followed by two drops
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Handbook of Ocular Disease Management - Bacterial Keratitis
every 30 minutes for 18 hours, and then tapered depending on patient response. Another fluoroquinolone,
ofloxacin 0.3% (Ocuflox) is also an effective treatment for bacterial keratitis. Both fluoroquinolones are as
effective at managing bacterial keratitis as fortified antibiotics, but with significantly fewer side effects.
To increase patient comfort and minimize inflammation, strong cycloplegia is mandatory. Begin with a
cycloplegic such as scopolamine 0.25% TID. If this is insufficient, switch to atropine 1% BID. Adjunctive use
of cold compresses will also help to reduce inflammation. If there is evidence of secondary inflammatory
glaucoma, Rx a topical beta-blocker BID.
Have the patient return daily for follow-up visits. Once the infection is controlled, add a topical steroid Q2H to
the regimen. Continue the daily follow-up and begin to taper all medications as you see improvement.
CLINICAL PEARLS
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If a patient presents with a corneal infiltrate but no overlying epithelial staining, the condition is not
bacterial keratitis. If there is epithelial breakdown but only minor inflammation and anterior chamber
reaction, then it most likely is not infectious bacterial keratitis.
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The inflammatory reaction is as damaging to the cornea as the infective organism. Once you've halted
bacterial proliferation, be sure to prescribe a steroid to speed healing and reduce corneal scarring. For
steroids to be beneficial, they must be used while the ulcer bed is still open, usually within the first 24
to 48 hours. If you wait until the ulcer re-epithelializes before adding a steroid, the beneficial effects
will be lost.
Other reports in this section
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Handbook of Ocular Disease Management - Bacterial Keratitis
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Herpes Simplex Keratitis
Herpes Simplex Keratitis
Signs and Symptoms
The keratitis caused by the herpes simplex virus (HSV) typically
presents as a unilateral "red eye" with a variable degree of pain or
ocular irritation. Photophobia and epiphora are common; however,
vision may or may not be affected, depending upon the location and
extent of the corneal lesion. You may see a vesicular skin rash and
follicular conjunctivitis with the initial infection, but these are less
common with recurrent HSV. A more common sign is secondary
uveitis.
A dendritic corneal ulcer is the hallmark sign of HSV infection, accompanied by stromal keratitis in more
severe presentations. These ulcers may begin as nondescript punctate keratopathies, but quickly coalesce to
form the familiar branching patterns which stain brightly with sodium fluorescein dye. Because the virus
invades and compromises the epithelial cells surrounding the ulcer, the leading edges (the so-called "terminal
end-bulbs") will stain with rose bengal or lissamine green.
Pathophysiology
Herpes simplex is actually the most common virus found in humans. It is transmitted via bodily fluids, usually
saliva, and may affect the skin and mucous membranes of the host. Primary infections occur most often in
children between the ages of 6 months and 5 years. It typically manifests as a vesicular rash, sometimes
affecting the skin of the lids but more commonly resulting in a "fever blister" or "cold sore" in or around the
mouth.
After resolution, the virus remains dormant in the body of the host and can be reactivated in as many as 25
percent of cases by fever, trauma, stress, immunosuppressive agents or exposure to ultraviolet radiation. In
recurrent attacks, the virus invades and replicates within the corneal epithelium. As the cells die, an ulcerative
keratitis results. Disciform stromal scarring, conjunctivitis and uveitis are common sequelae.
Management
Corneal epithelial disease secondary to HSV infection must be managed aggressively and quickly to prevent
deeper penetration. The treatment of choice is topical trifluridine 1% given at two hour intervals, nine times
daily. As the dendrites begin to regress, taper the dosage to q3-4h until the lesion resolves completely (usually
in seven to 10 days). At this point, however, have the patient continue the medication t.i.d. for another week to
ensure suppression of the virus.
Some practitioners recommend debriding the ulcer bed to remove active virus cells, but this has not been
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Herpes Simplex Keratitis
definitively proven to hasten resolution or improve the final visual outcome. You may also need to prescribe a
cycloplegic (homatropine 2% t.i.d.-q.i.d. or scopolamine 0.25% b.i.d.-q.i.d.), again depending upon the severity
of the uveitic response. Avoid topical steroids in cases of active epithelial HSV keratitis. Studies show that the
virus replicates more rapidly in the presence of steroids, prolonging the course of the disease. The use of oral
acyclovir (400mg 5x/day) or another oral antiviral for recalcitrant ulcers has yet to be proven clinically
significant. However, it has been shown recently that the use of oral acyclovir 400mg q.d. significantly reduces
the recurrence of herpes simplex keratitis in imunocompetent patients. At this point, consider using oral
prophylaxis therapy only in patients with confirmed recurrent HSV keratitis or patients on initial presentation
who request it after being thoroughly educated.
A new development in the management of herpes simplex keratitis has come in the form of topical acyclovir
ointment (Zovirax). Place the ointment in the lower cul-de-sac five times per day at four hour intervals. At this
point, toxicity seems to be low.
Clinical Pearls
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Suspect HSV in cases of unilateral adult-onset red eye that is inconsistent with the symptoms (i.e., the
patient seems to be in far less discomfort than the appearance of the eye would indicate), particularly if
the individual has a previous history of similar "infections."
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Each recurrent attack induces greater damage to the corneal nerves, leading to hypoesthesia (reduced
corneal sensitivity). The cotton-wisp test for corneal sensitivity is invariably positive in cases of HSV
keratitis; use it whenever in doubt. Also, consider a history of prolonged sun exposure or extreme
psychological stress to be significant in diagnosing HSV.
Other reports in this section
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Herpes Simplex Keratitis
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Herpes Simplex Keratitis
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Handbook of Ocular Disease Management - Phlyctenulosis
Phlyctenulosis
SIGNS AND SYMPTOMS
This nodular inflammation of the peri-limbal tissues occurs secondary
to an allergic hypersensitivity response of the cornea. The disease is
most common (60 percent of cases) in women during their first and
second decades who live in crowded or impoverished quarters.
Patients typically present with symptoms of tearing, ocular irritation, mild to severe photophobia and a history
of similar episodes. If the underlying cause is Staphylococcal infection, expect to see a rope-like, mucopurulent
discharge as well.
There are two distinct types of phlyctenular lesions: corneal and conjunctival. Under the slit lamp a conjunctival
(vascularized) phlyctenule appears as a 1 to 3mm hard, triangular, slightly elevated, yellowish-white nodule
surrounded by a hyperemic response, in the vicinity of the inferior limbus. These lesions tend to be bilateral.
Corneal phlyctenules produce more severe symptoms. They usually begin adjacent to the limbus as a white
mound, with a radial pattern of vascularized conjunctival vessels. The lesion may then migrate toward the center
of the cornea, progressing as a gray-white, superficial ulcer surrounded by infiltrate in the areas where the lesion
has been.
PATHOPHYSIOLOGY
The exact mechanism or mechanisms that produce phlyctenules is unclear. Histologically, they are composed of
lymphocytes, histocytes and plasma cells. Polymorphonuclear leukocytes are found in necrotic lesions. Their
formation seems to be the result of a delayed hypersensitivity reaction to tuberculin protein, Staphylococcus
aureus, Coccidioides immitis (a soil-based fungus common in the southwestern U.S.), Chlamydia, acne rosacea,
some varieties of interstitial parasites and the fungus Candida albicans. Rarely are cases idiopathic. Such a
diagnosis could only be made by exclusion.
MANAGEMENT
Ocular management begins with patient education to improve eyelid hygiene. Lid scrubs two to three times per
day along with artificial tears and ointments may soothe and reverse mild cases. Moderate to severe cases
require topical steroids or steroid-antibiotic combinations. Cycloplegia is only necessary if there is an associated
iritis. In most cases, prednisolone acetate (Pred Forte), one drop, Q2H/QID is sufficient, provided there are no
corneal contraindications.
If the suspected etiology is Staph. reaction or acne rosacea, prescribe 250mg of oral tetracycline QID or 250mg
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Handbook of Ocular Disease Management - Phlyctenulosis
erythromycin QID PO, along with topical antibiotic ointments such as bacitracin or erythromycin at bedtime.
Topical metronidazole (Metrogel) applied to the skin TID is also effective. Because tetracycline can damage
and discolor the teeth of children, it is contraindicated in patients under age 10. In these cases, substitute
doxycycline 100mg TID or erythromycin 250mg QID PO. Continue treatment for two to four weeks. In
suspicious cases, order a chest X-ray and PPD to rule out tuberculosis.
CLINICAL PEARLS
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Maintain the treatment as long as signs and symptoms persist, with follow-up visits weekly. Taper
steroids once you see improvement but maintain the antibiotic until the steroid therapy is completely
finished. Have patients continue the eyelid hygiene indefinitely.
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Other potential differential diagnoses include infiltrates secondary to chronic blepharitis, inflamed
pingueculum, herpes simplex and infectious or sterile corneal ulcer. The resurgence of tuberculosis
infection makes TB testing almost mandatory.
Other reports in this section
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Phlyctenulosis
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Handbook of Ocular Disease Management - Keratitis Sicca
KERATITIS SICCA / DRY EYE SYNDROME
SIGNS AND SYMPTOMS
As the name implies, patients with keratitis sicca or dry eye syndrome
typically present with complaints of dry, burning eyes and a "sandy"
or "gritty" foreign body sensation. Occasionally, patients will report
excess tearing (epiphora). Often, the symptoms are exacerbated by
poor air quality and low humidity, and are more prominent later in the
day. Upon inspection, most patients demonstrate a relatively white and
quiet eye. Key slit lamp findings include a negligible tear meniscus at
the lower lid and a reduced tear break-up time (TBUT), generally less
than ten seconds.
Fluorescein staining will usually reveal punctate epithelial keratopathy in the interpalpebral region. In severe
cases, the cornea and/or conjunctiva may also stain with rose bengal. Filaments-tags of mucus, epithelial cells
and tear debris-may also stain with fluorescein and rose bengal; filamentary keratitis is an extreme sequela of
keratitis sicca.
PATHOPHYSIOLOGY
Dry eye syndrome results primarily from compromise to either the quantity or quality of the precorneal tear
film. Tears are composed of a mucin layer, a water or aqueous layer, and an oil layer. Deficiencies in any one of
these components may create a tear film which is incapable of properly moistening the eye, resulting in
desiccation and symptomatic complaints. In addition, irregularities in the blink mechanism or conditions
affecting the regularity of the ocular surface (e.g., pterygia, keratoconus) may further interfere with proper
wetting of the cornea. Many drugs can also temporarily decrease lacrimal gland secretions, such as
antihistamines, phenothiazine anti-anxiety medications, oral contraceptives and atropine derivatives. Collagen
vascular disorders such as rheumatoid arthritis and Sjögren's syndrome also have a high association with dry eye
syndrome.
MANAGEMENT
Management is aimed at replenishing the eyes' moisture and/or delaying evaporation of the patient's natural
tears. Begin by recommending that the patient instill an ophthalmic lubricant every hour or more as needed, then
taper the therapy based upon patient response and compliance. A lubricating ointment used at bedtime may
provide additional comfort. For those patients who derive little relief from this therapy, or who fail to comply,
punctal occlusion may offer a more realistic and less complicated management strategy. First, test the patient's
response using dissolvable collagen plugs to ensure the therapy will provide relief from symptoms without
epiphora. If successful, occlude the inferior puncta using silicone plugs. In severe cases consider occluding both
the inferior and superior puncta, or recommend surgical cautery.
CLINICAL PEARLS
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Often, patients with dry eye syndrome are more symptomatic than their clinical signs would imply.
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Handbook of Ocular Disease Management - Keratitis Sicca
Typically, the diagnosis is based more on subjective complaints than slit lamp findings.
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Educate patients early and often that dry eye syndrome cannot be cured outright. Rather, the therapy
aims to control symptoms and reduce discomfort.
Other reports in this section
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Keratitis Sicca/Dry Eye Syndrome
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Handbook of Ocular Disease Management - Epithelial Basement Membrane Dystrophy
Epithelial Basement Membrane Dystrophy (EBMD)
SIGNS AND SYMPTOMS
EBMDs are bilateral, often asymmetrical corneal basement membrane
disorders usually occurring in individuals over 30. Symptoms vary,
ranging from nothing at all to mild, short-lived corneal irritation upon
waking with photophobia or glare.
Approximately 10 percent of affected individuals develop transient blurred vision with painful recurrent
epithelial erosions. Most patients experience fluctuating visual acuity without discomfort. Signs of EBMD
include corneal epithelial microcysts, whorling defects known as "fingerprints" or "mare's tails," and positive
and negative sodium fluorescein staining.
PATHOPHYSIOLOGY
A dystrophy is a non-infectious, non-inflammatory defect secondary to malnutrition or faulty metabolism.
There are four principle classes of corneal dystrophies:
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anterior dystrophies
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dystrophies of Bowman's layer
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stromal dystrophies
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endothelial dystrophies
Anterior EBMDs are variants of one cardinal pathophysiology. They are diagnosed and named principally by
their appearance. In EBMD disorders, the basal epithelial cells manufacture abnormal finger-like projections
that protrude from the abnormally thickened basement membrane. These projections reduce adherence of the
overlying epithelium, and produce the characteristic changes. Fibrogranular ridges associated with, and
adjacent to, these extensions form the fingerprint patterns. These protuberances bend in the epithelium,
trapping cells and intercellular debris to mold microcysts. When a series of microcysts become grouped
together and migrate forward, corneal surface abnormalities and RCE occur.
MANAGEMENT
The corneal changes of EBMD patients can be monitored closely with keratometry (paying specific attention to
mire quality) and biomicroscopy. Carefully assess the tear film and wetting stability of the corneal surface to
determine if keratitis sicca is present.
As opposed to the end of day symptoms of dry eye, the symptoms of EBMD are most severe in the morning.
Sodium fluorescein staining reveals surface irregularities and illuminates areas of positive staining (bright
green: missing epithelium) and negative staining (free of fluorescein: heaped epithelium). As an option, use
rose bengal or lissamine green to reveal areas of devitalized corneal cells.
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Handbook of Ocular Disease Management - Epithelial Basement Membrane Dystrophy
Treat asymptomatic patients with prophylactic supportive therapies. Artificial tear drops QID PRN, ointments
HS-TID, punctal plugs, blindfolds during sleep and goggles or spectacles that prevent dust exposure and add
ocular moisture retention support are helpful. Moderate presentations may require hypertonic drops and
ointments (NaCl 5%), Q3H to QID, for a minimum of six months. You can prescribe soft contact lenses to
smooth surface disturbances when intolerable levels of acuity exist in severe presentations.
Patients with acute recurrent corneal erosion may require debridement of the loose epithelium, topical
cycloplegia (cyclopentolate 1% TID or homatropine 5% BID), topical prophylactic antibiotic drops QID
(tobramycin, ofloxacin), or ointments and topical hypertonic drops and/or ointment. Manage pain with cold
compresses, oral analgesics or topical nonsteroidal anti-inflammatory preparations (Voltaren, BID to QID, or
Acular, BID to QID).
The long-term management of RCE follows the same course as EBMD. Cases of RCE that resist medical
management may require surgical procedures. Anterior stromal puncture (ASP) under topical anesthesia
involves the use of a 25g needle to place 0.1mm deep perforations, breaching Bowmans's membrane, at
0.25mm intervals in a chronic RCE zone in an attempt to initiate scar formation and healing. ASP can also be
achieved using the Nd:Yag laser. Dispense appropriate topical cycloplegic, antibiotic, steroidal and hypertonic
medications following the procedure. Pressure patching is also an option. Excimer photorefractive therapeutic
keratectomy (PTK) to smooth the corneal surface is an effective alternative modality.
CLINICAL PEARLS
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The use of the pressure patch remains controversial. While it is still considered acceptable, many
clinicians are electing not to patch, citing inability to medicate topically and inconvenience to the
patient. While contact lenses may be valuable for smoothing corneal surface irregularities, many
practitioners avoid them as bandage devices to keep therapy simple.
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There is no evidence suggesting topical nonsteroidal anti-inflammatory medicines increase healing
time.
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Since many sources suggest an autosomal dominant inheritance pattern, clinicians should closely
examine the family members of any EBMD patient.
Other reports in this section
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Handbook of Ocular Disease Management - Epithelial Basement Membrane Dystrophy
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Epithelial Basement Membrane Dystrophy (EBMD)
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Fuch's Endothelial Dystrophy
Fuchs’ Endothelial Dystrophy
Signs and Symptoms
Late hereditary (Fuchs’) endothelial dystrophy is usually seen
in the fifth or sixth decade of life. It is more common in
women than men, bilateral, and usually of dominant
inheritance. The dystrophy itself stems from the primary
malfunction of the corneal endothelium. This ultimately
29a.jpg (11920 bytes)
causes the disruption of the corneal dehydration system and
consequently a physiologically and optically compromised
tissue. Presenting symptoms include decreased vision, foreign
body sensation and pain upon waking. Biomicroscopic
findings include focal thickenings of the Descemet’s
membrane known as corneal guttata, corneal stromal edema,
folds in Descemet’s membrane secondary to corneal edema,
fine pigment dusting on the corneal endothelium, and in
advanced stages, corneal pannus, and bullous keratopathy. In general, corneal dystrophies exhibit familial
patterns and have no association with systemic or environmental factors. It is associated with a slightly
increased prevalence of open angle glaucoma.
Pathophysiology
The cornea consists of five discrete layers: epithelium, Bowman’s layer, stroma, Descemet’s membrane and
endothelium. When healthy, the endothelial cell layer is a single stratum of hexagonal cells that borders
Descemet’s membrane. It shows great metabolic activity and is actively involved in the maintenance of corneal
dehydration. Following trauma or injury, the surrounding endothelial cells slide over to the injured area. There
is no mitotic activity in the adult endothelium. This focal enlargement and/or change in shape of the endothelial
layers can be seen using special biomicroscopic techniques and is called polymegathism and pleomorphism,
respectively.
The clinical and histopathological progression of Fuchs’ is complex, but can best be divided into three stages,
which usually span 10 to 20 years. In the first stage the patient is initially asymptomatic, but manifests central
irregularly distributed guttata warts and geographically arranged pigment dusting. Occasionally, a diffuse
brown pigmentation of the central posterior surface is also seen. Histologically, the endothelial cells show
degeneration and deposition of abnormal Descemet’s membrane material.
In the second stage the patient develops stromal and epithelial edema, with symptoms of glare and hazy vision.
Visual acuity is usually 20/30 or better. As edema increases, the stroma thickens centrally, the opacity spreads
peripherally and the epithelium develops bullae, which correspond to intraepithelial lakes of fluid. As stromal
edema increases, Descemet’s membrane develops folds and vision falls. Eventually, the benefit of better vision
late in the day is lost, the epithelium becomes more bullous, and pain and photophobia develops.
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Fuch's Endothelial Dystrophy
In the third phase, subepithelial connective tissues appears centrally. This is an avascular tissue that does not
migrate in from the periphery like pannus, but arises in the central cornea. Clinically, it appears as an irregular,
dense, gray, swirling sheet of scar tissue. Histologically, it consists of active fibroblasts and of large and small
collagen fibrils between Bowman’s layer and the epithelium. In advanced cases, the stromal edema and
epithelial bullae disappear as the stroma scars, and the patient becomes more comfortable even though the
visual acuity is severely reduced.
Management
The treatment for Fuchs’ endothelial dystrophy varies, depending upon the severity of the disease, and may
range from hypertonic drops to surgical intervention. Patients with early stromal and/or epithelial edema may
be treated conservatively at first with 5% sodium chloride drops q.i.d. and 5% sodium chloride ointment at
bedtime. (Use of a hair dryer held at arms length from the surface of the cornea, in combination with the
hyperosmotic agents, may dry out the corneal surfaces and decrease the time the blur persists.)
A therapeutic soft lens (bandage lens) is beneficial in alleviating patient discomfort. A loosely fitting, flat, high-
water content soft contact lens will decrease the irregular astigmatism and the pain from ruptured epithelial
bullae. This mode of treatment has made life more pleasant for patients who could not afford corneal
transplants or who are awaiting a triple procedure with advancing cataract. Take note that any elevation of IOP
forces more fluid into the stroma across the compromised endothelium. Appropriate pressure reduction with
topical and or oral ocular antihypertensive medications may decrease the progression and symptoms secondary
to corneal edema. Corneal grafts for Fuchs’ dystrophy account for approximately 10 percent of all corneal
grafts performed. Generally, if the graft is performed before there is involvement of the peripheral cornea, there
is an 80 percent likelihood that the graft will remain clear for two years. Keratoplasty in eyes with narrow
angles should include lens removal to avoid angle closure with formation of peripheral anterior synechiae.
Patients with both Fuchs’ endothelial dystrophy and cataracts will do well with a combined penetrating
keratoplasty and cataract extraction.
Clinical Pearls
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Corneal guttata seen in young, asymptomatic patients are known as Hassall-Henle bodies and are of no clinical significance.
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Excessive central guttata in the absence of corneal edema is termed endothelial cell dystrophy. Endothelial cell dystrophy may remain
stable or progress to Fuchs’ dystrophy.
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Differential diagnosis should include posterior polymorphous dystrophy, which is a posterior corneal dystrophy with gray, hazy,
scalloped bands, variable corneal edema and iris involvement. Also consider aphakic and pseudophakic bullous keratopathy.
Other reports in this section
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Fuch's Endothelial Dystrophy
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Salzmann's Nodular Degeneration
Salzmann’s Nodular Degeneration
Signs and Symptoms
Most cases of Salzmann’s nodular degeneration present
asymptomatically. Discomfort does not usually occur until later
stages, at which time recurrent corneal erosion (RCE) may ensue.
Patients manifesting RCE typically report photophobia,
blepharospasm, tearing, and decreased acuity. In between bouts of
RCE, non-specific "dry eye" complaints such as burning or
grittiness are typical.
Clinically, Salzmann’s degeneration appears as an accumulation of bluish-white superficial nodules in the mid-
peripheral cornea. Generally, the eye is not inflamed unless there is associated corneal erosion. In that event,
there will be limbal injection, corneal edema, and an anterior chamber reaction.
There are conflicting reports regarding the laterality of Salzmann’s degeneration; an older study reports a
unilateral presentation in 80 percent of cases, while a more recent study suggests a bilateral predilection in 80
percent. The condition is seen more frequently in women than in men.
Patients with Salzmann’s degeneration usually describe a previous episode of ocular inflammation, often in
childhood. Associated disorders may include phlyctenular disease, vernal keratoconjunctivitis, trachoma, or
interstitial keratitis. Patients with a history of epithelial basement membrane dystrophy or corneal surgery may
also be at increased risk.
Pathophysiology
At the cellular level, the nodules seen in Salzmann’s degeneration represent clumped masses of collagen fibrils
anterior to Bowman’s membrane. Experts speculate that these peripheral accumulations of collagen are
produced by fibroblasts within the conjunctiva or limbal vessels. In some cases, transmission electron
microscopy has demonstrated reduplication of the epithelial basement membrane. Descemet’s membrane and
the corneal endothelium are characteristically unaltered, however.
One theory behind the development of Salzmann’s degeneration suggests that the inciting corneal inflammation
creates an irregular surface, allowing for uneven tear film distribution and exposure. A process known as
hyalization ensues, which is the same process responsible for the development of conjunctival pinguecula. As
the nodules grow in size, there is progressive damage and scarring at the level of Bowman’s membrane. This
ultimately results in epithelial erosion and potential impairment of acuity.
Management
Mildly asymptomatic cases of Salzmann’s degeneration may be managed with topical lubricants and/or a
bandage contact lens. Prophylactic antibiosis is advisable if epithelial defects are significant. In more severe
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Salzmann's Nodular Degeneration
cases, superficial keratectomy may be utilized to remove the nodules from the anterior cornea. Phototherapeutic
keratectomy (PTK) is also an option. If significant scarring is present, or if chronic epithelial breakdown makes
the condition unmanageable, lamellar or penetrating keratoplasty may be the only recourse.
Clinical Pearls
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The critical issue in managing Salzmann’s degeneration is proper diagnosis. Conditions such as band keratopathy, spheroid
degeneration (climatic droplet keratopathy), and corneal keloids may all present with a similar clinical appearance. Consult a corneal
specialist in those cases where diagnosis is elusive.
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It may be tempting to use topical corticosteroids in Salzmann’s degeneration, particularly if the patient is symptomatic. However,
since this condition is non-inflammatory in nature, steroids will have little effect. Additionally, the use of steroids introduces an
unnecessary risk in patients with a compromised epithelium.
Other reports in this section
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Handbook of Ocular Disease Management - Thygeson's Superficial Punctate Keratopathy
Thygeson's Superficial Punctate Keratopathy
SIGNS AND SYMPTOMS
The signs and symptoms of Thygeson's superficial punctate
keratopathy (SPK) are minimal. Patients usually report only a mild to
moderate foreign body sensation, tearing and occasionally
photophobia. There is no history of recent ocular inflammation, nor
typically any associated systemic illness. Upon gross inspection, the
affected eye appears normal, with little or no evidence of eyelid
swelling, conjunctival injection or corneal edema.
Biomicroscopy reveals numerous round or stellate areas of coarse, gray, slightly elevated intraepithelial
opacities. These lesions resemble subepithelial infiltrates, but are more superficial, duller in color, and less
organized. Also, these areas may demonstrate variable central staining with sodium fluorescein, whereas
subepithelial infiltrates typically do not stain. Inspection of the anterior chamber shows neither cells nor flare.
Visual acuity may be normal or mildly reduced, depending upon the density and location of the opacities.
Because Thygeson's SPK tends to run a chronic, remittent course, the patient may report similar experiences in
the past. The clinical presentation, although bilateral in nature, may be asymmetric, or involve only one eye at
a time.
PATHOPHYSIOLOGY
The etiology of Thygeson's SPK is unknown. Research indicates, however, that the condition may be caused
by a chronic subclinical viral infection affecting the deeper layers of the corneal basal epithelium. The
opacities represent corneal mononuclear cell infiltrates consistent with a viral entity. Studies have implicated a
varicella virus, possibly herpes zoster, as well as Chlamydia trachomatis in the development of Thygeson's,
although these claims are unsubstantiated.
In most cases, Thygeson's SPK presents with insidious onset. With or without treatment, the lesions will
eventually resolve; however, the disease often continues to plague these patients for months or even years, with
sporadic exacerbations. The trigger mechanism for these flare-ups appears to be idiopathic.
MANAGEMENT
Thygeson's SPK is a self-limiting disorder, but intervention usually speeds the resolution and enhances patient
comfort. Manage mild cases by recommending non-preserved artificial tear preparations, every two to three
hours while awake, with bland ophthalmic ointment at bedtime.
Treat more severe presentations with topical steroids, such as 0.1% fluorometholone alcohol (FML) or 1%
rimexolone (Vexol). In most cases, QID dosing is adequate, but increase dosage in severe cases if necessary.
Continue the treatment for one week, and then slowly taper therapy to avoid a rebound inflammation. Follow
up weekly during therapy, then every three to 12 months during remission.
CLINICAL PEARLS
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Handbook of Ocular Disease Management - Thygeson's Superficial Punctate Keratopathy
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Thygeson's SPK is enigmatic; it presents as a corneal inflammation associated with an essentially white
and quiet eye in an otherwise healthy patient. Other conditions that present with corneal infiltrates
usually induce at least a related conjunctivitis-the most common of these is epidemic
keratoconjunctivitis. Other entities in the differential include: bacterial keratoconjunctivitis, chlamydial
keratoconjunctivitis, toxic keratoconjunctivitis, exposure keratopathy and dry eye syndrome.
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Because of the chronic, remittent course of this disease, patients often present with their diagnosis "in
hand." Patients who are not already aware should be educated about the recurrent nature of Thygeson's
SPK, and the need for continued follow-up.
Other reports in this section
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Handbook of Ocular Disease Management - Acute Bacterial Conjunctivitis
Acute Bacterial Conjunctivitis
Signs and symptoms: The patient will present with injection of
the bulbar conjunctival and episcleral vessels, and perhaps also
the palpebral conjunctiva. Infection may begin in one eye and
subsequently spread to the fellow eye. There may be mild
photophobia and discomfort, but pain is not typical. There will be
fig01.jpg (5755 bytes)
concurrent mucopurulent discharge, and the patient usually
reports that the eyelids and eyelashes are matted shut upon
waking. Visual function typically is normal. The discharge is
corneotoxic and frequently results in a coarse punctate
epitheliopathy. Significant epitheliopathy may cause vision
Acute bacterial conjunctivitis
reduction and discomfort in some cases. Due to drainage of the
infection through the nasolacrimal system, there is no preauricular node involvement.
Pathophysiology: The eye has a series of defense mechanisms to prevent bacterial invasion.
These include bacteriostatic factors within the tears, the shearing force of the blink, an intact immune
system, and a population of normal colonizing non-pathogenic bacteria which competitively prevent
invasion by abnormal organisms. When these defense mechanisms break down, infection by
pathogenic bacteria can occur.
Invading bacteria, along with secreted exotoxins, represent foreign antigens which induce an antigen-
antibody immune reaction and subsequent inflammation. In a normal, healthy eye, the bacteria will
eventually be eradicated as the eye strives to return to homeostasis. However, the external load of
organisms can potentially set the eye up for corneal infection or involvement of other adnexal
structures. The most commonly encountered organisms are Staphylococcus aureus, Hemophilus
influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa.
In cases of hyperacute bacterial conjunctivitis, the patient will present with similar signs and
symptoms, albeit much more severe. The most common causative agents in hyperacute conjunctivitis
are Neisseria gonorrhoeae and Corynebacterium diptheroides. There is more danger in hyperacute
bacterial conjunctivitis as these organisms can penetrate an intact cornea.
Management: As in any bacterial infection, microbiologic studies with cultures and sensitivities is
the optimum means to reach a conclusive diagnosis. However, due to the expense of microbiologic
studies and relatively benign nature of the condition, most clinicians advocate the use of broad-
spectrum, empirical therapy and reserve culturing for hyperacute conditions or those that fail to
respond to initial therapy.
There are many options for empirical therapy. Excellent initial broad-spectrum antibiotics include
Ciloxan (ciprofloxacin, Alcon), Ocuflox (ofloxacin, Allergan), Quixin (levofloxacin, Santen), Polytrim
(polymixin B-trimethoprim, Allergan), gentamicin and tobramycin. These will give good coverage of
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Handbook of Ocular Disease Management - Acute Bacterial Conjunctivitis
gram-positive and gram-negative organisms, though the aminoglycosides (gentamicin and
tobramycin) have weak activity against Staphylococcal speciesand some strains of Pseudomonas
have been found to be resistant to the aminoglycosides. Polyantimicrobial therapy may be necessary
to cover all possible organisms initially. Soon-to-be-introduced fourth-generation topical
fluoroquinolones--moxifloxacin (Alcon) and gatifloxacin (Allergan)--have gram-negative coverage
similar to the existing fluoroquinolones but with enhanced coverage of gram-positive species. Use
these antibiotics qid to q1h, depending on the severity of the infection. Stress to patients that these
conditions are highly contagious.
Although antibiotics will eradicate the antigenic bacteria, they will do nothing to suppress the
concurrent inflammation. If there is no significant corneal disruption, then you can use corticosteroids
such as Pred Forte (prednisolone, Allergan), Flarex (fluorometholone, Alcon) or Lotemax (loteprednol,
Bausch & Lomb) concomitantly with the antibiotics to speed resolution of the inflammation. Steroid-
antibiotic combinations such as Maxitrol (neomycin-polymixin B-dexamethasone, Alcon), Pred-G
(gentamicin-prednisolone, Allergan), and Tobra Dex (tobramicin-dexamethasone, Alcon) are also
excellent initial choices for therapy when the cornea is intact.
Ocular Allergies: Oral or Topical Therapy?
Since the introduction of Livostin (levocabastine, Novartis Ophthalmics) in
1994, the eye-care market has seen an explosion of topical medications for
the treatment of allergic conjunctivitis. With no less than 12 prescription
topical agents now available, many eye-care practitioners and general
physicians still maintain that oral agents are necessary and even preferable
for treating moderate to severe allergic conjunctivitis.
Are oral medications better? These recent studies indicate that topical
medications may work as well or better than oral antihistamines:
• A study by the Fort Worth, Texas, Allergy & Asthma Association compared
two patient groups taking the nasal spray fluticasone proprionate (Flonase,
Glaxo Wellcome), and either Patanol or Allegra (fexofenadine, Hoechst
Marion Roussel). Patients taking Patanol experienced significantly less
itching and ocular injection than those using Allegra, and an equivalent
reduction in nasal symptoms in both groups.1
• Mark B. Abelson, M.D., showed that patients utilizing Claritin (loratadine,
Schering) demonstrated a significant reduction in ocular itching when
Patanol was added to the regimen.
• Researchers in Boston found that patients with normal ocular health who
took Claritin 10mg bid for four days were found to have increased keratitis
and conjunctival staining, decreased tear volume and break-up time, and
increased ocular discomfort when exposed to an adverse environment.3
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This research shows most patients are better served by topical anti-allergy
preparations for allergic conjunctivitis. Oral antihistamines with
diphenhydramine and chlopheniramine may compromise a patient's ability
to drive and work because of their sedating effects. Even those prescription
agents touted as "non-sedating," such as Claritin and Allegra, may
significantly impact ocular comfort and the ability to wear contact lenses
because of surface drying. As we all know, ocular irritation secondary to dry
eye is the single most common reason for discontinuation of contact lens
wear.
1. Lanier BQ, Abelson MB, Berger WE, et al. Comparison of the efficacy of combined
fluticasone propionate and olopatadine versus combined fluticasone propionate and
fexofenadine for the treatment of allergic rhinoconjunctivitis induced by conjunctival
allergen challenge. Clinical Therapeutics 2002;24(7):1161-74.
2. Abelson MB, Lanier BQ. Evaluation of Patanol and Claritin for allergic conjunctivitis
using the conjunctival antigen challenge. Poster presented at the annual meeting of the
American College of Allergy, Asthma, & Immunology; Philadelphia November 1998.
3. Nevius JM, Abelson MB, Welch D. The ocular drying effects of oral antihistamines
(Loratadine) in the normal population an evaluation. Poster presented at the annual
meeting of the Association for Research in Vision and Ophthalmology (ARVO); Fort
Lauderdale, Fla. May 1999.
Clinical pearls:
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Proper diagnosis is the hallmark of management of acute bacterial conjunctivitis. While
patients with bacterial conjunctivitis will report that their lids are matted shut in the morning with
mucopurulent material, patients suffering from viral and allergic conjunctivitis will sometimes
report similar experiences. However, the patients with viral and allergic conjunctivitis will
actually have crusting of the lashes due to drying tears and serous secretions; those with
bacterial conjunctivitis will manifest the wet, sticky, muco-purulent matting of the lashes. Too
often, clinicians consider the dry crusting of the lashes to be the same as the mucopurulent
matting and misdiagnose the condition.
●
Remember, due to the excellent defense systems of the external eye, acute bacterial
conjunctivitis is an uncommon condition.
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Do not taper antibiotics because this can lead to resistance. Once a condition resolves,
discontinue the therapy abruptly.
Other reports in this section
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Handbook of Ocular Disease Management - Allergic Conjunctivitis
Allergic Conjunctivitis
Signs and Symptoms: The human allergic response has
various objective signs and physical symptoms. Ocular allergic
conditions vary from the subtle signs of itchy, watery eyes with
mild hyperemia to extensive inflammatory interactions between
fig01.jpg (5755 bytes)
the ocular coats and adenexa. Symptoms typically include
itching, burning and tearing of the eyes with watery discharge. In
most cases the patient will report a history of allergies. The
important observable clinical signs include tissue swelling
(chemosis); red, edematous eyelids; conjunctival papillae; and a
Mild allergic conjunctivitis.
lack of a palpable preauricular node.
Pathophysiology: The allergic response is an overreaction of
the body's immune system to foreign substances known as
immunogens or allergens. The response can be innate or
acquired. The key component of the ocular allergic response is
the mast cell. When mast cells interact with specific allergens
they open like a lock being opened by a key--this is known as
degranulation--discharging chemical mediators into the
Severe allergic conjunctivitis with
surrounding tissues. The primary chemical mediators include
watch-glass conjunctiva.
histamine (which is responsible for increased vascular
permeability, vasodilation, itching, bronchial contraction and increased mucus secretion); neutral
proteases (which generate other inflammatory mediators); and arachidonic acid (a crucial component
of the cyclooxygenase pathway).
Management: Because there are many levels of ocular allergic reactions, management is primarily
aimed at reducing symptoms. The most effective treatment for allergic conjunctivitis is to eliminate the
potentially offending allergen, although this is not usually possible. Cold compresses, artificial tears
and ointments soothe, lubricate and wash away or dilute the antigens on an as-needed basis.
Topical decongestants produce vasoconstriction, reducing hyperemia, chemosis and other symptoms
by retarding the release of the chemical mediators into the tissues from the blood stream. The topical
antihistamines--Emadine (emedastine, Alcon) and Livostin (levocabastine, Novartis)--and oral
antihistamines are also excellent therapies. Mast-cell stabilizers--Alamast (pemirolast, Santen), Alocril
(nedocromil, Allergan), Alomide (lodoxamide, Alcon) and cromolyn sodium--inhibit release of the
histamine, but will take longer to relieve symptoms. The dual action medications--Patanol
(olopatadine, Alcon Laborato-ries), Zaditor (ketotifen, Novartis) and Optivar (azelastine, Bausch &
Lomb)--combine antihistamines with mast-cell stabilizing properties. Clinicians use them widely for
managing symptoms associated with seasonal allergies.
The topical nonsteroidal anti-inflammatory drugs--such as Acular (ketorolac, Allergan) and Voltaren
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(diclofenac, Novartis)--may offer relief in moderate cases; topical steroids--such as Pred Forte
(prednisolone, Allergan) and Lotemax (loteprednol 0.5%, B&L)--are typically reserved for more severe
presentations. Alrex (loteprednol 0.2% B&L) is a topical steroid specifically indicated for the
management of allergic ocular reactions. It is effective even in severe ocular allergic responses and
appears to be safe for long-term management of ocular allergies. Still, you should monitor IOP in
patients who take the drug for 10 days or more.
Ocular Allergies: OTC or Rx?
Even though there a dozen FDA-approved prescription topical medications to treat
allergic conjunctivitis, the American public still purchases more than 40 million
bottles of over-the-counter (OTC) ophthalmic preparations each year. More
individuals use agents such as Opcon-A (Bausch & Lomb) and Visine-A (Pfizer) for
allergy-related ocular itching than any of the prescription medications.
OTC products combine a topical decongestant, such as naphazoline hydrochloride,
with a topical antihistamine such as pheniramine maleate or antazoline phosphate.
Patients are lured by the promise of "fast, effective relief from red, itchy eyes." As
clinicians, we must ask, "Can they possibly work as well as drugs such as Patanol or
Zaditor?"
On the contrary, we know that the OTC preparations are generally less effective for
managing ocular allergies, because the antihistamines in the OTC agents are not as
potent and are formulated at much weaker concentrations than those in the Rx
agents. In fact, we know that OTC agents can actually be harmful in some
individuals. Studies have shown that chronic use of topical vasoconstrictors such as
naphazoline can result in toxic, follicular reactions and contact dermatitis.1
So why do so many patients still use OTC eye drops? Most likely there are two
factors at play: Cost and ignorance. On average, OTC drops cost about $5-$10 for a
15ml bottle, while newer drugs such as Patanol, Zaditor or Optivar may cost
between $50 and $60 or more for a 5ml bottle. Patients see the cost savings, but
they remain unaware that OTC drops are less efficacious and are potentially
detrimental to their ocular health.
It's our obligation to educate patients regarding the OTC products they may
encounter, as well as prescribe the best and most appropriate therapies for them.
Patients need to know that OTC allergy solutions may be fine on occasion for those
who suffer a mild exposure, but should not be used in the continuous management
of seasonal or perennial allergic conjunctivitis.
1. Soparkar CN, Wilhelmus KR, Koch DD, et al. Acute and chronic conjunctivitis due to over-the-
counter ophthalmic decongestants. Arch Ophthalmol 1997;115(1):34-8.
Clinical Pearls:
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●
Advise patients with a history of seasonal allergic conjunctivitis to try to avoid the substances
that precipitate symptoms. In severe cases, these patients may be treated four weeks in
advance with loading doses of topical mast-cell stabilizers (Alomide, Alamast, Alocril or
cromolyn sodium), or mast cell-stabilizing antihistamines (Patanol, Zaditor or Optivar) to retard
the degranulation process.
●
Follow patients on a topical NSAID agent for 1-2 weeks after starting therapy. Patients placed
on topical steroidal preparations should return for follow-up one week after starting therapy.
●
Optimal therapy for ocular allergies includes an antihistamine, mast-cell stabilizer and a
steroid. This combination will address all aspects of the allergic inflammatory reaction.
●
Newer mast-cell stabilizers (Alamast and Alocril) are patient-friendly in that they can be dosed
bid (although Alamast is indicated for qid dosing).
Other reports in this section
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Allergic Conjunctivitis
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Handbook of Ocular Disease Management - Viral Conjunctivitis
Viral Conjunctivitis
(Pharyngoconjunctival Fever & Epidemic Keratoconjunctivitis)
Severe Follicular Reaction
A Pseudomembrane in EKC
SIGNS AND SYMPTOMS
Most viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe,
disabling visual difficulties. The two most common self-limiting forms of viral conjunctivitis are epidemic
keratoconjunctivitis and pharyngoconjunctival fever.
Pharyngoconjunc-tival fever (PCF) is characterized by fever, sore throat and follicular conjunctivitis. It may be
unilateral or bilateral. It is caused regularly by adenovirus 3 and occasionally 4 or 7. Corneal infiltrates are rare.
The disorder varies in severity but usually persists for four days to two weeks. While the virus is shed from the
conjunctiva within 14 days, it remains in fecal matter for 30 days.
Epidemic Keratoconjunctivitis (EKC) often presents as a bilateral, inferior, palpebral, follicular conjunctivitis,
with epithelial and stromal keratitis. Subepithelial corneal infiltrates are much more common in EKC than in
PCF and are typically concentrated in the central cornea. EKC is regularly caused by adenovirus types 8 and 19.
The key clinical signs of both conditions include: conjunctival injection, tearing, serous discharge, edematous
eyelids, pinpoint subconjunctival hemorrhages, pseudomembrane formation and palpable preauricular lymph
nodes. In severe cases, conjunctival desiccation causes scarring and symblepharon formation (adherence of the
bulbar and palpebral conjunctivas).
Both conditions are highly contagious. Patients will usually report recent contact with someone who had either
red eyes or an upper respiratory infection. Both forms tend to start in one eye, then spread to the other eye within
a few days. In rare cases, the focal subconjunctival hemorrhages can evolve into acute hemorrhagic
conjunctivitis.
PATHOPHYSIOLOGY
Viral conjunctival infections are thought to be caused by airborne respiratory droplets or direct transfer from
one’s fingers to the conjunctival surface of the eyelids. After an incubation period of five to 12 days, the disease
enters the acute phase, causing watery discharge, conjunctival hyperemia and follicle formation. Lymphoid
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Handbook of Ocular Disease Management - Viral Conjunctivitis
follicles are elevated, with avascular lesions ranging from 0.2 to 2mm in size. They have lymphoid germinal
centers that have responded to an infectious agent.
Adenovirus type 8 can proliferate in the corneal epithelial tissues, producing the characteristic keratitis and
subepithelial infiltrates. This, along with the immune response to viral antigens, causes lymphocytes to collect in
the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These
are made up of fibrin and leukocytes, and in prolonged cases, of fibroblast and collagen deposits.
“Pseudomembranes” are much easier to remove than “true” membranes.
MANAGEMENT
Because EKC and PCF are contagious and self-limiting, the primary treatment once again is patient education.
Instruct patients to stay home from work or school until there is absolutely no discharge. Also instruct them not
to share utensils, glasses, linens or wash cloths with others.
Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g.,
naphazoline) and steroids (Vexol, Flarex, Pred Forte) two to four times daily. If a membrane is present, peel it
off with a wet, cotton-tipped applicator or forceps. After removal, prescribe a topical antibiotic-steroid
combination such as Tobradex or Maxitrol q.i.d. Anti-viral drugs such as Viroptic are ineffective against
adenovirus.
Recently, there has been a breakthrough in the management of adenoviral keratoconjunctivitis. Cidofovir
(Vistide), an anti-viral drug used intravenously to treat cytomegalovirus retinitis, appears to be effective in
adenoviral keratoconjunctivitis. The topical form creates a faulty viral DNA structure. Twice daily instillation is
recommended. This topical anti-viral is also possibly effective against herpes simplex and zoster, and Epstein-
Barr virus.
CLINICAL PEARLS
●
Keep your equipment, instruments and chair area meticulously clean to avoid contaminating your
patients and staff.
●
Most practitioners reserve topical steroidal therapy for severe cases (if the infection is on the visual axis
and affecting acuity, for example), or recalcitrant cases. EKC infiltrates resolve without scarring the
cornea.
●
Tell patients to expect the symptoms to get worse for about seven to 10 days before getting better, and
that the infection won’t completely go away for three to six weeks. Remember to always taper steroids
slowly as the condition recedes.
Other reports in this section
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Viral Conjunctivitis
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Toxic Conjunctivitis
Toxic Conjunctivitis
Signs and Symptoms
Toxic conjunctivitis, sometimes referred to as toxic follicular
conjunctivitis, is a syndrome that results when the palpebral
and bulbar conjunctiva have been chronically exposed to any
number or combinations of foreign substances. The process
may occur unilaterally or bilaterally, depending upon
exposure. Its clinical features include the presentation of
ocular itching, burning and tearing, injection of the bulbar
and palpebral conjunctivae, chemosis, along with inferior
and or superior eyelid follicle and papillae formation, and an
absence of preauricular lymphadenopathy. Keratopathy is
often present secondarily. In chronic cases, pannus formation
may result.
Typically, patients present with a history of using or starting
an ocular medication for an episode of presumed bacterial or
viral conjunctivitis only to find that the ocular symptoms and
signs continue to increase despite correct usage of the
medicine. The term medicamentosa is applicable here; it
connotes a reaction to the preservatives in medications, or
the medications themselves, producing a more substantial
keratitis.
Pathophysiology
The toxic/allergic response is an over-reaction of the body’s immune system to immunogens or allergens. The
response can be innate or acquired. A variation of this over-reaction is manifested when the body responds
hyperactively to exogenous materials such as medicines, contact lenses, contact lens solutions, dust, dander or
viral shedding. Overactivity of this type is commonly referred to as a toxic or allergic reaction. With respect to
the eye and its adnexa, the result is toxic conjunctivitis.
The key component to the ocular allergic response is the mast cell. When mast cells interact with specific
allergens, like a lock being opened by a key, they open (degranulation) discharging chemical mediators into the
surrounding tissues. The primary chemical mediators include histamine (responsible for increased vascular
permeability, vasodilation, bronchial constriction and increased secretion of mucous), neutral proteases
(generating other inflammatory mediators) and arachidonic acid (crucial component of the cyclooxygenase
pathway leading to production of prostaglandins and leukotrienes).
There are four types of hypersensitivity reactions.
●
Type I reactions are immediate hypersensitivity reactions or anaphylactic reactions. These reactions
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Toxic Conjunctivitis
produce sudden degranulation of mast cells mediated by the antibody IgE.
●
Type II reactions involve the body’s ability to distinguish itself from non-self. Abnormalities in this
element of the system give rise to autoimmune disease.
●
Type III reactions involve combinations of antigen and antibody known as immune complexes.
Offending triggers may be intrinsic (i.e. a protein molecule) or extrinsic (a penicillin molecule) and
produce a significant tissue response in an attempt to rid the area of the invader.
●
Type IV reactions, sometimes referred to as cell mediated hypersensitivity reactions, involve the T-
lymphocytes and lymphokines. The reaction is classically delayed until sufficient antigens stimulate the
chemical cascade. In the ocular tissues, these chemical exchanges incite conjunctival and adnexal
vasodilation, chemosis, edema and lacrimation. Individuals experience pain, itching, swelling and
irritation. The discharge produced is typically serous and the conjunctival findings include follicles
(hyperplasia of lymphoid tissue within the eyelid stroma) and papillae (hyperplastic palpebral
conjunctival epithelium infiltrated by lymphocytes and plasma cells).
Management
Management is primarily aimed at reducing symptomatology. Cold compress, artificial tear drops and ointments
soothe and lubricate. Topical decongestants produce vasoconstriction, reducing hyperemia, chemosis and other
symptoms by retarding the release of the chemical mediators into the tissues from the blood stream. Topical
antihistamines (Emadine, Livostin, b.i.d. to q.i.d.) and oral antihistamines (Benadryl, 25 to 50mg, p.o. t.i.d.) are
also excellent therapies for acute signs and symptoms. Mast cell stabilizers such as cromolyn sodium (Opticrom)
and lodoxamide tromethamine (Alomide) may be useful in seasonal or chronic cases. The non-steroidal anti-
inflammatory drugs (NSAIDS: Acular, Voltaren, b.i.d. to q.i.d.) may offer relief in moderate cases, while topical
steroid preparations (Alrex, Lotemax, FML, FML Forte, Allergan, Pred Mild, Pred Forte, Flarex, Vexol, b.i.d. to
q.i.d., and Inflamase Mild and Forte, b.i.d. to q.i.d.) are reserved for the most symptomatic presentations.
Clinical Pearls
●
Toxic/allergic conjunctivitis is a diagnosis that can be made based upon history and course. Typically,
vision is unaffected despite its unruly appearance. You can usually identify a causative source as the
precipitator of the acute signs and symptoms. Even if left untreated, toxic conjunctivitis often begins to
resolve within seven days.
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In true toxic conjunctivitis, there will not be a palpable preauricular lymph node.
Other reports in this section
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Conjunctivitis with Pseudomembrane
Conjunctivitis with Pseudomembrane
Signs and Symptoms
Often, conjunctivitis is discovered by most patients in the
morning, when they notice, upon waking, that their eyelids are
"stuck together." The classic signs and symptoms of
conjunctivitis include ocular redness secondary to palpebral
14a.jpg (23410 bytes)
and or bulbar conjunctival injection, irritation, itching,
lacrimation, discharge, and possibly keratitis with decreased
vision. Conjunctival follicular and papillary response,
discharge, subepithelial infiltration, subconjunctival
hemorrhage, corneal epitheliopathy, symblepharon formation
and lymphadenopathy are variables dictated by the etiology.
Pathophysiology
A true membrane forms when the fibrinous excretory or inflammatory exudate that is secreted by invading
microorganisms or ocular tissues permeates the superficial layers of the conjunctival epithelium. True
membranes become interdigitated with the vascularity of the conjunctival epithelium. They are firmly adherent,
and tearing and bleeding often result when removed. B-hemolytic streptococci, Neisseria gonorrhoeae,
Corynebacterium diphtheriae, Stevens-Johnson syndrome (severe systemic vesiculobullous eruptions affecting
the mucous membranes-erythema multiforme) and chemical or thermal burns are among the common etiologic
sources.
Pseudomembranes consist of coagulated exudate that is loosely adherent to the inflamed conjunctiva. They are
typically not integrated with the conjunctival epithelium and can be removed by peeling, leaving the
conjunctival epithelium intact. Their removal produces little if any bleeding. Epidemic keratoconjunctivitis
(EKC), ligneous conjunctivitis (a rare idiopathic bilateral membranous/pseudomembranous conjunctivitis seen
in children with thick, ropy, white discharge on the upper tarsal conjunctiva), allergic conjunctivitis, and
bacterial infections are the primary causes.
Epidemic keratoconjunctivitis (EKC) often presents as a bilateral, inferior palpebral, follicular conjunctivitis,
with epithelial and subepithelial keratitis and normal corneal sensation. It is extremely contagious. The
subepithelial infiltrates (SEI) are typically concentrated in the central cornea. Mild EKC is regularly caused by
adenovirus virus serotypes 1, 2, 3, 4. The more severe form of the disease is caused by virus serotypes 5, 8, 19
and 37.
Pharyngoconjunctival fever (PCF) is characterized by history of fever, sore throat, upper respiratory infection,
and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and 7. The
cornea is rarely affected and infiltrates are uncommon. While the virus is shed from the conjunctiva in 14 days,
it remains in fecal excretion for 30 days. This may explain why some epidemics center around swimming pools
in summer. The disorder varies in severity and may persist for four days to two weeks.
Management
In most cases, because viral conjunctivitis is contagious and self-limiting, the primary function of management
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is to increase patient awareness and comfort by providing education and decreasing symptomatology. Patients
should be kept home from work or school until contagious discharge is eliminated. Patients should be warned
not to use common utensils or linens.
If pseudo- or true membranes are present, debride them using a wet cotton-tipped applicator or forceps. Include
supportive therapies such as cold compress and topical tear solutions, topical vasoconstrictors (Naphcon A),
topical NSAID preparations (Acular, Voltaren), and topical steroids (Flarex, Pred Forte, Vexol) b.i.d. to q.i.d.
Topical antibiotic/steroid combination therapy (Tobradex, Maxitrol) QID is indicated if the infection has a
suspected bacterial source. Cycloplegia is only necessary in the most severe cases. When you suspect bacterial
etiology, conjunctival scrapings may provide differential diagnostic information.
A new drug is on the horizon for treating entities causing pseudomembraneous conjunctivitis. Cidofovir, a
topically applied DNA analog, has been proven clinically efficacious in the treatment of adenoviral
conjunctivitis and epidemic keratoconjunctivitis and is currently awaiting approval for commercial use.
Clinical Pearls
●
The four clinical features that must be considered in the differential diagnosis of any conjunctival
inflammation include:r
- Type of discharge (watery, mucoid, purulent, mucopurulent)
- Type of conjunctival reaction (follicular or papillary)
- Presence or absence of membrane or pseudomembrane formation
- Presence or absence of lymphadenopathy (association with sexually transmitted or viral origin)
●
Epidemic viral conjunctivitis, epidemic keratoconjunctivitis (EKC) and pharyngoconjunctival fever
(PCF) can be caused by a number of different viruses and are probably the most common causes of
pseudomembranous conjunctivitis.
Other reports in this section
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Giant Papillary Conjuncctivitis
Giant Papillary Conjunctivitis
Signs and Symptoms
Giant papillary conjunctivitis (GPC) is a common condition
frequently seen in soft contact lens patients, patients with
exposed suture knots, and patients with prostheses. Patients
with asthma, hay fever or animal allergies may be at greater
risk. The etiology of GPC may be immunological, where
contact lens deposits act as allergens.
16a.jpg (19021 bytes)
Initial presentation may occur months or even years after lens wear has been initiated. The papillae in GPC can
be observed on the superior tarsus and (by definition) measure 1mm in diameter. Ocular itching after lens
removal, increased mucus discharge in the morning, photophobia and decreased lens tolerance are all initial
symptoms. Vision can be affected either as an artifact of the deposits on the lens, due to lens displacement
secondary to superior lid papillary hypertrophy, or repetitive mechanical corneal abrasion with infiltration
(shield ulceration).
Pathophysiology
The allergic response is considered to be an over-reaction of the body’s immune system to immunogens or
allergens. This response can be innate or acquired after multiple exposures to a particular antigen.
The GPC response has no seasonal variation. While the histamine level of tears is increased in vernal
keratoconjunctivitis (VKC), it remains level in GPC. Despite this difference, VKC and GPC are
pathophysiologically similar. Cytologic scrapings from the conjunctiva of patients with GPC exhibit an
immunologic response containing lymphocytes, plasma cells, mast cells, eosinophils and basophils suggesting
an antigen-antibody mechanism. The action of phospholipase A2 secondary to the allergic response causes the
release of histamines via the degranulation of mast cells. This increases capillary permeability, produces
lymphocyte circulation (T-cells, eosinophils, and monocytes) and initiates the liberation of arachidonic acid,
which is a catalyst for the cyclooxygenase and lipoxygenase pathways. These pathways produce inflammatory
mediators such as thromboxanes, leukotrienes and prostaglandins that cause the discomfort and formation of the
papillae.
Management
Management is primarily aimed at reducing symptoms. In more serious cases, aggressive management may be
required to prevent ocular tissue damage. The type and frequency of medications depends upon the severity of
the condition. Topical supportive therapies act to supplement the biological tears, to wash away debris and
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Giant Papillary Conjuncctivitis
environmental allergies. The flushing away of allergens and other debris plays an obvious role in reducing or
even canceling the GPC response. Examples of such products include Bion Tears, Tears Naturale Free, Refresh
Plus, Ocucoat PF and Dry Eye Therapy.
Topical mast cell stabilizers are a tested and proven modality for treating GPC. Topical mast cell stabilizers are
the treatment of choice for chronic GPC. They work by stabilizing the receptors on mast cell vesicles before they
can degranulate, beginning the cycle of the allergic response. VKC, atopic keratoconjunctivitis (AKC), and GPC
all respond well. If the patient’s history is well known for GPC, a 10-day loading period preceding the onset of
symptoms with a preparation like cromolyn sodium (Opticrom, Crolom), at a dosage of four to six times daily, is
usually effective in stalling or preventing the initial stages of the disease. Following this, you may need to
continue therapy for four to six weeks or until the end of the episode. Another mast cell stabilizer made available
in recent years is lodoxamide (Alomide). Like cromolyn sodium, it is a safe drug and is used in the same manner
for a wide variety of allergic conditions, at a dosage of two to four times a day. Olopatadine (Patanol) combines
mast cell stabilization with antihistamine properties and may be the best therapy due to its dual role. Another
advantage of Patanol is its twice daily dosing.
Mast cell stabilizers have been shown to deliver significant therapeutic impact on the GPC reaction. However, to
ease chronic irritations of this type, the most effective method remains eradication of the antigen.
In recalcitrant cases, topical corticosteroids function to deliver potent, palliative mediation by reducing the
inflammatory response. Topical corticosteroids reduce capillary permeability, suppress lymphocyte circulation,
inhibit the degranulation of mast cells, reduce the numbers of basophils and neutrophils, and decrease the
production of prostaglandins, thromboxanes and leukotrienes. GPC resistant to standard therapies may respond
to topical steroids. Excellent choices of steroids for management of GPC include Vexol, Lotemax, and Alrex.
Clinical Pearls:
●
Patients with allergic symptoms often have dry eyes as their primary problem. Make sure to rule out tear
deficiency in chronic GPC conditions.
●
When topical steroids are required, you can typically prescribe them four and six times a day for up to
seven days to achieve control and then taper off.
●
The final alternative may entail fitting susceptible patients with daily disposable or rigid gas-permeable
lenses, or even discontinuing contact lens wear altogether.
●
Daily disposable soft contact lenses in combination with medical therapy are an excellent compromise
for the patient who absolutely cannot discontinue lens wear for any reason.
Other reports in this section
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Handbook of Ocular Disease Management - Vernal Keratoconjunctivitis (VKC)
Vernal Keratoconjunctivitis (VKC)
Signs and symptoms: VKC is a chronic, bilateral inflammation
of the superior and limbal palpebral conjunctiva. The warmer the
climate, the greater its prevalence. Onset typically occurs
between ages 3 and 25 years. Males typically are affected more
fig01.jpg (5755 bytes)
than females.
Symptoms often include severe itching with thick, ropy discharge.
In most cases, patients have a history of allergies or infantile
eczema. The important clinical signs include large conjunctival
A classic presentation of VKC.
papillae on the back of the superior tarsus; raised Horner-Trantas
dots (gelatinous, white clumps of degenerated eosinophils usually located at the superior limbus);
areas of superficial punctate keratitis (SPK) and, in severe cases, well-demarcated, sterile corneal
shield ulcers, located superiorly. You can differentiate VKC from atopic keratoconjunctivitis (AKC)
based on age, location, dermatitis and lack of seasonal variability.
Pathophysiology: Allergic responses are the immune system's overreaction to foreign substances
known as immunogens or allergens. The key component of the vernal ocular allergic response is the
eosinophil. Vernal conjunctivitis, which is IgE-mediated, is the only ocular disease to involve solely
Type I hypersensitivity. Involvement of secondary inflammatory cells--particularly eosinophils (along
with mast cells) resident to the substantia propria of the superior tarsus--can produce sequelae.
Papillae with epithelial downgrowth form crypts, at the base of which lie mucus-producing goblet cells.
Plasma cells and lymphocytes collect inside papillae stroma. Vernal shield ulcers develop in the
upper regions of the cornea. The base of the ulcer is composed of abnormal mucus, fibrin and serum,
deposited as a gray plaque. Friction secondary to the roughened superior conjunctiva erodes the
corneal epithelium.
Management: Management of VKC is primarily aimed at reducing symptoms and preventing serious
vision-threatening sequelae. The most effective treatment is to eliminate or avoid the allergen;
however, this is often impractical. Cold compresses and artificial tears and ointments soothe, lubricate
and may dilute the antigen. Topical decongestants such as naphazaline and phenylephrine produce
vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release of
chemical mediators. Topical antihistamines--Livostin, Patanol, Zaditor, Optivar--and oral
antihistamines--Benadryl, 25mg tid--are also excellent therapies. Mast-cell stabilizers such as
Alomide, Alocril, Alamast and cromolyn sodium can be useful before the disease flares or to keep it
under control following acute treatment; however, mast-cell stabilizers often do little to abate the
symptoms. NSAIDS such as Acular and Voltaren bid-qid may offer relief in moderate cases, with
topical steroidal preparations--Pred Forte, Lotemax, Alrex or Pred Mild (prednisolone 0.12%,
Allergan) bid-qid--reserved for more severe presentations.
Patients with shield ulcers should receive additional treatment involving aggressive cycloplegia
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Handbook of Ocular Disease Management - Vernal Keratoconjunctivitis (VKC)
(atropine 1%, homatropine 5% or scopolamine 0.25%, bid) and topical antibiotic drops--Tobrex
(tobramycin, Alcon), Ciloxan (ciprofloxacin, Alcon); Ocuflox (ofloxacin, Allergan), Quixin (levofloxacin,
Santen) or Polytrim (trimethoprim/polymyxin B, Allergan). Also consider prescribing the mucolytic
acetylcysteine (Mucomyst 10% or 20%), q4-6h. A low-water-content, thin hydrogel lens can reduce
the interaction between the lid and cornea. When the corneal lesion re-epithelializes, you can then
initiate topical steroids.
Clinical Pearls:
●
In cases that occur chronically, consider treating in advance with loading doses of topical mast-
cell stabilizers (Alomide, Alamast, Alocril or cromolyn sodium) or mast-cell-stabilizing
antihistamines (Patanol or Zaditor). This is an attempt to retard the degranulation process, thus
slowing, eliminating or reducing the debilitating consequences. If this is effective, maintain this
therapy throughout the allergy season.
●
Remember that mast-cell stabilizers will not affect the current symptoms but will instead lessen
future reactions.
●
Follow patients placed on supportive therapies (artificial tears or cold compresses) on an as-
needed basis. Those receiving topical medications should return at one week, with close
monitoring afterward. Patients on top ical steroids should undergo periodic IOP measurement.
Patients treated for shield ulceration should return for follow-up every 1-3 days.
Other reports in this section
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Superior Limbic Keratoconjunctivitis
Superior Limbic Keratoconjunctivitis (SLK of Theodore)
Signs and Symptoms
Individuals presenting with SLK typically report symptoms of
ocular discomfort, including burning, foreign-body sensation,
or non-descript pain. Additionally, patients may complain of
photophobia and excessive tearing. Gross clinical signs often
include mild lid swelling and pseudoptosis as well as
blepharospasm. Visual acuity is usually not affected.
Inspection of the ocular surface in SLK reveals a sectoral inflammation and injection of the superior bulbar
conjunctiva. The limbal margin of the cornea may be inflamed as well. Eversion of the upper lid reveals a
uniform papillary hypertrophy along the tarsus, which may be mild to marked. Vital dye staining is standard in
SLK, with patients displaying punctate epithelial disruption of the affected region; this is evident with both
sodium fluorescein dye as well as rose bengal or lissamine green solutions. Filaments are encountered within the
precorneal tear film in roughly half of all patients with SLK. The condition is typically bilateral but often
asymmetric. In most instances, the diagnosis of SLK is based solely upon the characteristic presentation. The
only known laboratory confirmation is the presence of keratinized epithelial cells from scrapings of the affected
superior bulbar conjunctivae.
Pathophysiology
The exact etiology and pathogenesis of SLK remains unclear. Infectious agents such as bacteria, viruses, fungi,
and other intracellular parasites appear to be unrelated to this condition. An autoimmune etiology has been
considered, based upon the pattern of the disorder (i.e., exacerbations and remissions), the female predominance,
and an association with thyroid disease and other autoimmune diseases.
The most widely accepted theory regarding the pathogenesis of SLK is that it results from mechanical irritation
of the superior limbal region, as loose conjunctival tissue rubs against the limbus during blinking. Factors such
as tight lids, prominent globes, and thyroid disease have been offered as potential instigators of this reaction.
A newer theory regarding the etiology of SLK implicates a local tear deficiency to the superior
keratoconjunctiva. Researchers have proposed that this deficiency results in significantly reduced levels of vital
tear-based nutrients to the affected region, as well as increased mechanical friction from the superior lid.
Management
SLK is a chronic, recurrent and sometimes recalcitrant disorder. While no treatment has yet been shown to be
100 percent effective, many modalities have been employed successfully. The treatment of choice for most
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Superior Limbic Keratoconjunctivitis
practitioners has been 0.5 to 1.0% silver nitrate solution, applied topically to the superior bulbar and tarsal
conjunctivae. This treatment chemically cauterizes the irregular tissue, promoting regrowth of new, healthy
epithelium. Unfortunately, recurrences have been known to occur after using silver nitrate, and retreatments are
common.
Pressure patching has been employed for severely symptomatic cases of SLK, as well as the use of subsequent
bandage hydrogel lenses to alleviate the mechanical irritation. Thermal cauterization as well as surgical
recession or resection of the superior bulbar conjunctiva has also been employed as treatment modalities for
SLK. The use of topical preparations, including vitamin A eyedrops, 4% cromolyn sodium solution, and
Alomide (0.1% lodoxamide tromethamine solution, Alcon) have also been somewhat effective in managing
SLK. Most recently, lacrimal punctal occlusion therapy has been advocated for this disorder.
Clinical Pearls
●
In managing this disorder, topical agents should be employed in the early stages of all mild and moderate
presentations; thermocautery, chemocautery, and surgical resection should be employed only when less
invasive means have failed.
●
Lacrimal occlusion therapy may prove to be a viable option for SLK; while additional research is needed
in this area, recent studies have shown great potential.
●
SLK of Theodore should not be confused with contact lens-induced SLK (CL-SLK), a condition that is
occasionally observed in young, otherwise healthy hydrogel lens wearers. An association with
thimerosal-preserved solutions has been seen in some of these patients. The typical presentation of CL-
SLK consists of increasing contact lens intolerance, superior tarsal and bulbar injection, and significant
superior corneal staining with stromal hazing. Corneal involvement may be noted as far inferiorly as the
superior pupillary margin. Treatment for CL-SLK consists of temporarily discontinuing contact lens
wear, along with the liberal use of preservative-free ocular lubricants. Upon resolution, contact lens wear
may be resumed with a fresh pair of lenses, however all thimerosal-preserved solutions should be
terminated. In more severe or recurrent cases, patients may need to be refit with RGP materials.
●
Refer all patients presenting with SLK for a systemic workup, including a serologic thyroid panel. A
1995 study demonstrated a 65 percent correlation between SLK and systemic thyroid disease. Other
disorders such as rheumatoid arthritis and Sjögren’s syndrome may also have similar associations.
Other reports in this section
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Superior Limbic Keratoconjunctivitis (SLK of Theodore)
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Handbook of Ocular Disease Management
PHLYCTENULOSIS (PHLYCTENULAR KERATOCONJUNCTIVITIS)
Signs and Symptoms
Phlyctenular keratoconjunctivitis is a nodular inflammation of the
perilimbal tissues that occurs secondary to an allergic
hypersensitivity response of the cornea.16 The disease has a
worldwide distribution and is most often seen in the first and
second decades in women (60%) living in crowded or
impoverished quarters. The disease has been associated with
systemic disorders such as Behçet's disease, tuberculosis, HIV
and rosacea among others.46 Patients typically present with
symptoms of tearing, ocular irritation, mild to severe photophobia
Inferior temporal phylectenule.
and a history of similar episodes.13,6 If the underlying cause is
staphylococcus, a rope-like, mucopurulent discharge may be present.2
There are two distinct types of phlyctenular lesions: corneal and conjunctival. Biomicroscopic
evaluation of a conjunctival (vascularized) phlyctenule reveals a 1mm to 3mm, hard, slightly elevated,
yellowish-white nodule, surrounded by a hyperemic response, in the vicinity of the inferior limbus. The
lesions tend to be bilateral. Corneal phlyctenules produce more severe symptoms. They usually begin
adjacent to the limbus as a white mound, with a radial pattern of vascularized conjunctival vessels on
the conjunctival side.2 The lesion may then migrate toward the center of the cornea, progressing as a
gray-white, superficial ulcer surrounded by infiltrate in the areas where the lesion has been.16
Pathophysiology
The exact mechanism by which phlyctenules are produced is unclear. Histologically, they are
composed of lymphocytes, histocytes and plasma cells. Polymorphonuclear leukocytes are found in
necrotic lesions.2 Their formation seems to be the result of a delayed hypersensitivity reaction to
tuberculin protein, Staphyloccocus aureus, Coccidioides immitis, Chlamydia, ocular rosacea, some
varieties of interstitial parasites, or Candida albicans.13 Rarely are cases idiopathic; such a diagnosis
should be made by exclusion.
Management
Ocular management of phlyctenular keratoconjuntivitis begins with patient education to improve
eyelid hygiene. Lid scrubs two to three times a day, along with artificial tears and ointments, may
soothe and reverse mild cases. Moderate to severe cases require topical steroidal or steroidal/
antibiotic combination medicines. Cycloplegia is only necessary if significant inflammation is present.
In mild cases, lid scrubs and copious lubrication may suffice. In most cases, prednisolone acetate
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(Pred Forte, Allergan), one drop, q2h-qid is sufficient. A combination agent such as Tobradex is an
excellent option. If the suspected etiology is staph or rosacea, 250mg of oral tetracycline qid or
250mg erythromycin qid, along with topical antibiotic ointments such as bacitracin or erythromycin hs,
should be added.6 Additionally, topical metronidazole (Metrogel, Galderma) applied to the skin tid is
also effective. Because tetracycline can damage and discolor the teeth of children, it is
contraindicated in persons under the age of 10. Here, doxycycline, 100mg tid, or erythromycin 250mg
qid po, may be substituted.13,6 Treatment should continue for two to four weeks. In suspicious cases,
a chest X-ray, PPD, HIV titre and HLA typing (BehcetHLAB51) should be obtained.16
Clinical Pearls
●
Maintenance doses of oral and topical steroids and antibiotics may continue to relieve patients'
signs and symptoms. This practice is acceptable, provided that the patient tolerates the
regimen. Weekly follow-up is recommended. Once significant improvement is noted, the
steroid should be tapered. The antibiotic coverage should continue, prophylactically, until the
steroid is removed. Eyelid hygiene should be maintained indefinitely.13,5,6
●
Other potential differential diagnoses include infiltrates secondary to chronic blepharitis,
inflamed pingueculum, herpes simplex and infectious or marginal corneal ulcer.13, 6
FOURTH-GENERATION FLUOROQUINOLONES: COMBATING OR
PROMOTING BACTERIAL RESISTANCE?
FEW WOULD ARGUE that the fluoroquinolones represent the most potent and
beneficial antibiotic agents currently available. Whether for peri-operative
prophylaxis or management of bacterial ocular infection, fluoroquinolone
antibiotics are clearly the market leader at this time. These drugs work by
inhibiting the function of crucial bacterial enzymes involved in cellular replication.
This leads to disruption of the DNA, which prevents bacteria from replicating,
resulting in rapid death of the invading organisms.
The fourth-generation fluoroquinolones include Vigamox (0.5% moxifloxacin,
Alcon) and Zymar (0.3% gatifloxacin, Allergan). They differ chemically and
pharmacologically from previous generations with respect to side chains located
at the C-7 and C-8 positions. These side chains impart enhanced bactericidal
activity and prevent bacterial defenses from rendering the drugs inert.
Subsequently, these new drugs display excellent intrinsic activity against both
common and atypical bacterial pathogens. And, while many common bacterial
strains are known to have developed resistance to older fluoroquinolones such as
ciprofloxacin and ofloxacin,1 these organisms appear to be fully susceptible to the
new fourth-generation fluoroquinolones.
Research has demonstrated that these new drugs are significantly more potent
against a wide range of bacterial pathogens.2,3 In addition, at least one of the new
fourth-generation fluoroquinolones, Vigamox, boasts improved dosing (tid vs. qid),
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Handbook of Ocular Disease Management
higher concentration (0.5% vs. 0.3%), more neutral pH (6.8 vs. 4.5 to 6.0), and
absence of added preservatives such as benzalkonium chloride. Clearly, with all
these advantages, what could possibly deter the eye care community from
immediately adopting this medication as the new drug of choice?
Unfortunately, many have expressed hesitation to begin utilizing the new fourth-
generation fluoroquinolones like Vigamox and Zymar for fear of creating new,
resistant strains of bacteria.
After all, it has been less than 15 years since Ciloxan and Ocuflox were
introduced, and we are already seeing significant resistance to these drugs.
Hence, some argue that if we use our new "big guns" on routine ocular infections,
rather than reserve them for severe infections, we will promote and accelerate the
process of resistance.
While virtually all antibiotics are subject to resistance over time, the new fourth-
generation fluoroquinolones stand the best chance of overcoming this trend. By
their very design, they have been engineered to defy bacterial resistance. Older
fluoroquinolones are known to target the enzyme DNA gyrase (topoisomerase II)
in Gram-negative bacteria, and topoisomerase IV in Gram-positive bacteria. By
contrast, the new fourth-generation drugs have the capacity to block both of these
enzymes simultaneously in both Gram-positive and Gram-negative bacteria; this
means that, for resistance to occur, mutations would have to occur
simultaneously at two sites rather than just one. Another characteristic of the new
drugs helps to combat bacterial efflux, a process by which the pathogens actively
pump the drugs out of the cytoplasm. The surest way to prevent resistance is to
not use doses below that recommended in the product insert. Antibiotics should
not be tapered. They should be used to their desired effect and then abruptly
discontinued. Using sublethal dosing will lead to resistance. For example,
Vigamox is dosed tid. Dosing should not be below tid.
No one can predict the future, but one observation can be made with relative
confidence--the continued use of older, second- and third-generation
fluoroquinolones will certainly not help to overcome the current trends in bacterial
resistance. The fourth-generation fluoroquinolones, on the other hand, offer our
current patients the best possibility for a positive outcome. Whether for surgical
prophylaxis or the treatment of bacterial ocular infection, drugs such as Vigamox
and Zymar deserve serious consideration.
1. Goldstein MH, Kowalski RP, Gordon YJ. Emerging fluoroquinolone resistance in
bacterial keratitis: A 5-year review. Ophthalmology 1999; 106(7):1313-8.
2. Mather R, Karenchak LM, Romanovski EG, et al. Fourth-generation fluoroquinolones:
New weapons in the arsenal of ophthalmic antibiotics. Am J Ophthalmol 2002; 133
(4):163-6.
3. Kowalski RP, Dhaliwal DK, Karenchak LM, et al. Gatifloxacin and moxifloxacin: An in
vitro susceptibility comparison to levofloxacin, ciprofloxacin, and ofloxacin using
bacterial keratitis isolates. Am J Ophthalmol 2003; 136(3):500-5.
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1. Cullom RD, Chang B. Cornea : Phylectenulosis. In : Cullom RD, Chang B. The Wills Eye Manual: Office and
Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia, PA: J.B. Lippincott Co. 1994;64-
65.
2. Wagoner MD, Bajart AM, Allansmith MR. Phlyctenulosis. In: Fraunfelder FT, Roy FH Current Ocular
Thearapy 3. Philadelphia, PA ; W.B. Saunders Co. 1990 :454-456.
3. Schimmel DJ. Infiltrative Keratitis. In: Onofrey, B.E. Clinical Optometric Pharmacology and Therapeutics.
Philadelphia, PA: J.B. Lippincott Co. 1994; 1-13.
4. Hochedez P, Zeller V, Truffo, C, et al. Lymph-node tuberculosis in patients infected or not with HIV:
general characteristics, clinical presentation, microbiological diagnosis and treatment. Pathol Biol 2003; 51
(89):496-502.
5. Hashida N, Ohguro N, Yamamoto S, et al. Unusual neutrophil infiltration under the soft contact lens in a
patient with Behcet's disease. Jpn J Ophthalmol 2003; 47(5):469-72.
6. Blaustein BH, Gurwood AS. Recurrent phlyctenular keratoconjunctivitis: a forme fruste manifestation of
rosacea. Optometry 2001; 72(3):179-84.
Other reports in this section
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Handbook of Ocular Disease Management
ACUTE ALLERGIC CONJUNCTIVITIS
Signs and Symptoms
Allergic conjunctivitis represents the single most common form of
ocular allergic disease.1 Acute allergic conjunctivitis describes
the abrupt and immediate response seen in sensitized individuals
after exposure to a particular allergen or sensitizing agent. Two
forms are recognized: seasonal allergic conjunctivitis (SAC),
which coincides with pollen blooms such as ragweed, and
perennial allergic conjunctivitis (PAC), in which exposure may
occur at any time throughout the year (e.g., allergies to cat
dander or dust mites). In the majority of cases, allergic
conjunctivitis is a bilateral phenomenon, but may be asymmetric.
Mild allergic conjunctivitis.
The allergic response classically involves several signs and symptoms, all of which may vary in
intensity. Ocular itching remains the hallmark symptom; tearing is also an exceedingly common
complaint, particularly after rubbing the eyes in response to itching. More severe reactions may
prompt symptoms of ocular burning, foreign-body sensation or photophobia, though these are
relatively rare. Clinical evaluation reveals variable conjunctival hyperemia and chemosis. Ocular
discharge is watery, though mucus may accumulate in the fornices or collect on the lash margin in the
form of "crusts," especially during sleep. Eversion of the eyelids may reveal a fine papillary response,
particularly along the upper tarsal plate. Externally, the eyelids may be red, swollen and edematous,
with a pseudoptosis in pronounced cases. A palpable preauricular lymph node is noticeably absent. If
questioned, the patient will often reveal a personal or family history of allergies. Concurrent symptoms
of allergic rhinitis, post-nasal drip, or sinus congestion may be present, especially in SAC.
Pathophysiology
The allergic response is classically considered to be an over-reaction of the body's immune system to
foreign substances (allergens). The response can be innate or acquired. The key component to the
ocular allergic response is the mast cell. When mast cells interact with specific allergens, the cell
membrane opens, much like a lock being opened by a key. This response is known as degranulation,
and the process causes a discharge of chemical mediators into the surrounding tissues. The primary
chemical mediator released during degranulation is histamine, which is responsible for increased
vascular permeability, vasodilation, bronchial contraction and increased secretion of mucus. Heparin,
chymase, tryptase and other substances are also released from mast cells. In severe or prolonged
allergic reactions, a "late- phase" response may occur in which cell membranes begin to break down
into arachidonic acid, which is further degraded to form prostaglandins, leukotrienes and
thromboxane (powerful mediators of inflammation that initiate stimulation of pain receptors and
migration of white blood cells). This late phase is far more common in disorders such as atopic and
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vernal keratoconjunctivitis, however. In acute allergic conjunctivitis, less than 2% of cases show this
type of severe inflammatory reaction.2
Management
The management of ocular allergic reactions is primarily aimed at reducing symptomology and
quelling any significant inflammation. The most effective treatment for allergic conjunctivitis is
elimination or avoidance of the potentially offending allergen, although this may not always be
possible or practical. Artificial tear solutions serve to soothe, lubricate and flush or dilute the antigens
from the ocular surface; these may be used on an as-needed basis. Cold compresses and topical
decongestants help to produce vasoconstriction, reducing hyperemia, chemosis and other symptoms
by retarding the release of the chemical mediators into the tissues from the blood stream.
Decongestant solutions (containing one of the following: naphazoline, antazoline, tetrahydrozaline or
phenylephrine) are available as over-the-counter preparations, either alone or in combination with a
mild topical antihistamine (e.g. pheniramine maleate or antazoline phosphate). These agents are the
treatment used by the vast majority of patients with ocular allergies who self-medicate. Unfortunately,
these OTC preparations have been associated with significant tachyphylaxis as well as chronic
follicular conjunctivitis and eczematoid blepharoconjunctivitis.3,4 An OTC medication that may give
palliative relief without the adverse effects of the decongestant solutions is the homeopathic allergy
eye drop Similisan #2.
A variety of prescription ophthalmic medications are
available for the management of allergic conjunctivitis.
Overall, five distinct classes or categories of topical
drugs are recognized; these include: (1) antihistamines,
e.g. Livostin (0.05% levocabastine hydrochloride,
Novartis) and Emadine (0.05% emedastine dif umarate,
Alcon); (2) mast cell stabilizers, e.g. Opticrom (4%
cromolyn sodium, Allergan), Alomide (0.1% lodoxamide
tromethamine, Alcon), Alocril (2% nedocromil sodium,
Allergan), and Alamast (0.1% pemirolast postassium,
Moderate allergic conjunctivitis with
Santen); (3) antihistamine/mast cell stabilizer
chemosis.
combinations, e.g. Patanol (olopatadine hydrochloride,
Alcon), Zaditor (ketotifen fumarate, Novartis), and
Optivar (0.05% azelastine hydrochloride, Bausch &
Lomb); (4) corticosteroids, e.g. Alrex (0.2% loteprednol
etabonate, Bausch & Lomb), Vexol (1% rimexolone,
Alcon), and Pred Forte (1% prednisolone ace-tate,
Allergan); and (5) non-steroidal anti-inflammatory agents
(NSAIDs), e.g. Acular (0.5% keto-rolac tromethamine,
Allergan). In general, all of these medications are
Severe allergic conjunctivitis with watch
beneficial to some degree. Topical antihistamines
glass crystal conjunctiva.
provide prompt symptomatic relief, but their effects are
short-lived (i.e., ~ 6 hours). Mast cell stabilizers prevent degranulation and hence eliminate the
allergic response, but they may take several days to a week in order to achieve full efficacy.
Antihistamine/mast cell stabilizer combinations provide the benefits of both of these categories and
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are by far the most common choice among eye care practitioners; these drugs also have the unique
advantage of bid dosing, as compared to most other medications, which require qid administration.
Topical corticosteroids may serve to quell inflammation and offer relief to those patients with more
severe, late-phase responses, although this is relatively rare with acute allergic conjunctivitis.2 Also,
the risk of cataractogenesis and ocular hypertension with prolonged use of topical corticosteroids is
well known. Topical NSAIDs are likely the least effective options for ocular allergy. While they may
provide mild symptomatic relief, they do not directly address mast cell degranulation or the histamine
response, and inhibit only a portion of the inflammatory cascade. Oral antihistamines are rarely
required for the treatment of acute allergic conjunctivitis, unless there is associated rhinitis, sinusitis,
urticaria, or other manifestations of systemic allergy. Some of the older, over-the-counter
antihistamines such as Benedryl (diphenhydramine hydrochloride 25mg, Parke-Davis) and Chlor-
Trimeton (chlorpheniramine maleate 8mg, Schering-Plough), are effective but can induce drowsiness
and functional impairment.5,6 In late 2002, loratadine 10mg, formerly a prescription medication, was
approved by the FDA as an over-the-counter product under various trade names, including Claritin,
Alavert, Tavist ND, and Dimetapp ND. This drug is considered to be a non-sedating antihistamine,
similar in efficacy to other prescription medications such as Clarinex (desloratadine 5mg, Schering-
Plough), Allegra (fexofenadine 60mg and 180mg, Aventis), and Zyrtec (cetirizine 5 and 10mg, Pfizer).
The sedative effect of these drugs is greatly diminished as compared to drugs such as
diphenhydramine, though it is not entirely eliminated. Other side effects also exist with systemic
antihistamines that are not of concern with topical agents. Most importantly, orals may predispose
patients to dryness of the mucosal membranes of the mouth, nose and eyes.7
Expect to see at least two new allergy medications sometime after 2004: Elestat (0.05% epinastine
hydrochloride) is a new antihistamine/mast cell stabilizer combination from Inspire, which received
FDA approval in October 2003. In addition, Alcon has developed a 0.2% formulation of olopatadine
hydrochloride (Patanol) for once-daily use.
Clinical Pearls
●
When evaluating patients with presumed allergic conjunctivitis, pay attention to the inferior
fornix and medial canthus. In many cases, the caruncle and plica semiluminaris may
demonstrate marked hyperemia or inflammation. This is presumably because of the
accumulation of histamine-laden tears in the area of the lacrimal puncta.
●
In differentiating allergic conjunctivitis from other forms of ocular surface disease, a helpful
question may be "What happens when you rub your eyes?" Most "itchy" surface disorders
such as dry eye and blepharitis generally improve with digital manipulation, because it
stimulates the flow of additional tears. However, allergy is a vascular mediated event; rubbing
the eyes creates vasodilation, which induces further release of histamines and other toxins into
the ocular tissues. Hence, patients with true allergies almost always say their symptoms
worsen when they rub their eyes.
●
Given the vast array of excellent topical prescription medications now available for allergic
conjunctivitis, practitioners have little reason to ever recommend over-the-counter
decongestant products. There is evidence that these OTC products are quite inferior and
potentially harmful.4
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Seasonal allergic conjunctivitis usually occurs around the same time each year, and may last
for only a month or two. Therefore, patients who present for examination during other times of
the year may go undiagnosed. It is important to ask not only whether the patient is
experiencing symptoms at the time of the exam, but also if they ever suffer from red, itchy,
watery eyes. The safety and efficacy of today's medications allow for proactive prescribing,
even months before symptoms arise.
OVERVIEW OF NEW OCULAR ALLERGY PRODUCTS
IT IS ESTIMATED that millions of Americans suffer from ocular allergies. In 2003,
there were no less than 12 FDA-approved prescription topical medications for the
treatment of allergic conjunctivitis: Acular, Alamast, Alocril, Alomide, Alrex,
Crolom, Emadine, Livostin, Opticrom, Optivar, Patanol and Zaditor. In 2004,
however, Elestat (epinastine HCl 0.05% ophthalmic solution, Inspire Pharma-
ceuticals) became available as an ocular allergy medication, and we can expect
another new choice: a new once-daily formulation of Patanol (0.2% olopatadine
HCl ophthalmic solution, Alcon).
Elestat is a topically active, direct H1-receptor antagonist and an inhibitor of the
release of histamine from the mast cell. It is selective for the histamine H1-
receptor but also has affinity for the H2 receptors. Essentially, it is the fourth drug
in the same family as Patanol, joining the ranks of Zaditor and Optivar. Clinical
studies have shown it to be safe and effective in patients three years of age and
older, and it was found not to be significantly superior to levocabastine (Livostin)
for controlling symptoms of ocular itching when administered twice daily.1,2 Other
studies demonstrated a rapid onset of action within three to five minutes after
conjunctival antigen challenge, and the duration of effect was shown to be
approximately eight to 12 hours.3
The new 0.2% formulation of olopatadine HCl promises to be a truly unique
addition to the ocular allergy arena. At double the concentration of the original
Patanol, this new agent offers true once-daily dosing for sufferers of allergic
conjunctivitis. Studies show that 0.2% olopatadine possesses a rapid onset-of-
action, a prolonged duration of action, and is safe and well tolerated.4,5 Studies
also demonstrate that this formulation effectively controls the signs and symptoms
associated with allergic conjunctivitis for at least 16 to 24 hours post-instillation.5
The future will likely see even more products introduced to combat ocular
allergies. Cyclosporine A (Restasis, Allergan), which was approved for the
treatment of keratoconjunctivitis sicca in 2003, may someday be a treatment
option for allergic conjunctivitis. A recent study showed that management of
allergic conjunctivitis with topical cyclosporine had a satisfactory evolution in 83%
of patients, with 50% experiencing symptomatic relief with the first week of
treatment.6
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With all of these new considerations, the pharmaceutical industries will no doubt
be promoting their products heavily in 2004. With more direct-to-consumer
marketing, patients may inquire about a new treatment option. It is our obligation
to be familiar with these agents and to be proactive in choosing the best therapy.
1. Torkidsen GL, Paradis AJ, Welch DL, et al. Safety evaluation of ophthalmic
epinastine HCl in a healthy pediatric population. Poster presented at the14th
Congress of the European Society of Ophthalmology (SOE); Madrid, Spain. June,
2003.
2. Abelson MB, Ghosh P, Bradford R, et al. Safety and efficacy of ophthalmic epinastine
in patients with allergic conjunctivitis. Poster presented at the 60th Anniversary
Meeting of the American Academy of Allergy, Asthma, & Immunology; Denver, CO.
March, 2003.
3. Crampton HJ, Abelson MB, Gomes P, et al. Efficacy and safety of ophthalmic
epinastine evaluated by conjunctival allergen challenge. Poster presented at the14th
Congress of the European Society of Ophthalmology (SOE); Madrid, Spain. June,
2003.
4. Abelson MB, Gomes P, Welch DL. Olopatadine reduces ocular signs and symptoms
associated with allergic conjunctivitis 16 hours after instillation. Poster presented at
the annual meeting of the Association for Research in Vision and Ophthalmology
(ARVO); Fort Lauderdale, May 2003.
5. Greiner JV, Spindel GP, Gomes PJ, et al. Olopatadine is effective for the prevention
and treatment of the signs and symptoms of allergic conjunctivitis. Poster presented
at the annual meeting of the Association for Research in Vision and Ophthalmology
(ARVO); Fort Lauderdale, May 2003.
6. Velasco P, Baca O, Velasco R, et al. Topic cyclosporine "A" in the management of
allergic conjunctivitis. Poster presented at the annual meeting of the Association for
Research in Vision and Ophthalmology (ARVO); Fort Lauderdale, May 2003.
1. Abelson MB, George MA, Garofalo C. Differential diagnosis of ocular allergic disorders. Ann Allergy 1993; 70
(2):95-107.
2. Hingorani M, Calder V, Jolly G, et al. Eosinophil surface antigen expression and cytokine production vary in
different ocular allergic diseases. J Allergy Clin Immunol 1998; 102(5):821-30.
3. Abelson MB, Butrus SI, Weston JH, Rosner B. Tolerance and absence of rebound vasodilation following
topical ocular decongestant usage. Ophthalmology 1984; 91(11):1364-7.
4. Soparkar CN, Wilhelmus KR, Koch DD, et al. Acute and chronic conjunctivitis due to over-the-counter
ophthalmic decongestants. Arch Ophthalmol 1997; 115(1):34-8.
5. Gengo F, Gabos C, Miller JK. The pharmacodynamics of diphenhydramine-induced drowsiness and changes
in mental performance. Clin Pharmacol Ther 1989; 45(1):15-21.
6. Bower EA, Moore JL, Moss M, et al. The effects of single-dose fexofenadine, diphenhydramine, and placebo
on cognitive performance in flight personnel. Aviat Space Environ Med 2003; 74(2):145-52.
7. Welch D, Ousler GW 3rd, Nally LA, et al. Ocular drying associated with oral antihistamines (loratadine) in
the normal population - an evaluation of exaggerated dose effect. Adv Exp Med Biol 2002; 506(Pt B):1051-
5.
Other reports in this section
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CONJUNCTIVAL CONCRETIONS (OCULAR LITHIASIS)
Signs and Symptoms
Conjunctival concretions, or lithiasis, are seen as small, white to yellow nodules superficially buried within and beneath the palpebral
conjunctiva. They may occur in either the upper or lower lid; when inferior, they often appear adjacent to or underlying fluid-filled
conjunctival cysts. These small, round, calculi appear to be a side effect of an aging palpebral conjunctiva, or a sequela of recurrent
episodes of chronic conjunctivitis. They have been associated with chronic atopic keratoconjunctivitis and Herbert's pits following post-
trachomatous degeneration.1,2 However, they frequently occur idiopathically.
The patient with lithiasis may report a foreign-body sensation that is especially prominent upon blinking, although most patients are
asymptomatic. The concretions typically remain buried, benign and unnoticed by patients until or unless they enlarge, at which time
they may protrude through the palpebral tissues. Contact with the cornea leads to foreign-body sensation, as well as epithelial
Concretions embedded in palpebral
disruption and a potential reduction in acuity if the visual axis is involved.
conjunctiva.
Pathophysiology
Conjunctival concretions have been described as inclusion cysts filled with keratin (a protein constituent of epidermis and hair) and epithelial debris within the inferior and superior
palpebral conjunctiva. However, research has confirmed that there is a granular, membranous nature to the masses, which are composed mainly of mucinous secretions of
transformed conjunctival glands admixed with degenerated epithelial cells.3 Histochemically, concretions have been found to stain strongly for phospholipid and elastin, weakly for
polysaccharides and negatively for amyloid, iron and glycogen.2
Ironically, there is very little calcium integrated within the accumulated material, as previously thought.2
Management
Concretions do not generally require interventional management as long as patients remain asymptomatic and the cornea is undamaged. All patients should be appropriately
educated as to the etiology and prognosis of this disorder. Those who are mildly symptomatic may be palliated by the use of artificial tear solutions and/or ointments.
In more severe cases--where palpebral tissues are at risk for damage, corneal erosion has occurred or symptoms have developed, persisted or worsened--excision is the modality
of choice. This may be accomplished in-office by applying an anesthetic-soaked cotton tipped applicator over the area and using a small gauge (e.g., 25gto 27g) needle to excavate
and extract the small calculi. Jewelers' forceps may be very useful in gripping the concretions once the conjunctiva has been breached. In exceedingly superficial cases, simple
manipulation with a cotton-tipped swab may be sufficient to loosen the nodule. After removal, the subsequent use of an antibiotic-steroid ointment (e.g., Tobradex, Alcon) helps to
minimize iatrogenic inflammation and prevent infection.
Clinical Pearls
●
Conjunctival concretions are avascular, granular, yellow-white masses that resemble crystals, and are visible upon lid eversion. Differ-ential diagnoses include amyloid
deposits, internal hordeola, adeno-chrome deposits, debris and foreign matter or tumor.
●
Concretions typically respond favorably to excision and normally do not recur after removal, but recurrence is a possibility of which patients should be educated.
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As a conservative estimate, perhaps only one patient in 50 with concretions ever requires surgical removal.4
1. Chumbley LC. Herbert's pits and lid concretions: An important association. Eye 1988; 2 (Pt 5):476-7.
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2. Chin GN, Chi EY, Bunt AH. Ultrastructural and histochemical studies of conjunctival concretions. Arch Ophthalmol 1980; 98:720-4.
3. Chang SW, Hou PK, Chen MS. Conjunctival concretions. Polarized microscopic, histopathologic, and ultrastructural studies. Arch Ophthalmol 1990; 108(3):405-7.
4. Kulshrestha MK, Thaller VT. Prevalence of conjunctival concretions. Eye 1995; 9 (Pt 6):797-8.
Other reports in this section
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Handbook of Ocular Disease Management - Chlamydial & Gonococcal Conjunctivitis
Chlamydial & Gonococcal Conjunctivitis
SIGNS AND SYMPTOMS
Chlamydial (inclusion) conjunctivitis typically affects sexually active
teens and young adults and is the most frequent infectious cause of
neonatal conjunctivitis in the U.S. The Centers for Disease Control
(CDC) recognizes chlamydia as one of the major sexually transmitted
pathogens, estimating approximately three million new cases per year.
Women seem to be more susceptible than men. The incidence of
infection seems to be directly related to sexual activity and geography,
with urban populations having higher incidences. The incidence in
pregnant women overall is 4 to 10 percent.
Diagnosis of inclusion conjunctivitis is often difficult. Many times there are little, if any, symptoms. Infants
whose mothers have untreated chlamydial infection have a 30 to 40 percent chance of developing neonatal
chlamydial conjunctivitis. Systemic signs and symptoms may include a history of vaginitis, pelvic inflammatory
disease or urethritis.
Ocular signs and symptoms include the chief complaint that an eye infection has persisted for over three weeks
despite treatment with topical antibiotics. Conjunctival injection, superficial punctate keratitis, superior corneal
pannus, peripheral subepithelial infiltrates, iritis and follicles (most dense in the inferior cul-de-sac) may all be
present. Mucopurulent, stringy or mucus discharge is common. A palpable preauricular node is almost always
present.
Gonococcal conjunctivitis, sometimes referred to as hyperacute conjunctivitis, is also a sexually transmitted
ocular disease. While sexual contact is the customary route of transmission, even casual interaction with infected
individuals has been reported as a cause. Newborn infants may acquire the infection by passing through an
infected birth canal. Systemically, gonococcal infections are associated with infection of the urethra, cervix and
rectum. Symptoms vary from nothing to discharge and irritation.
This unusually contagious ocular disease typically presents as a hyperacute red eye of less than four weeks
duration with foreign body sensation; the eye may be “glued” shut with severe purulent discharge. The
conjunctivitis has an incubation period of two to seven days. Conjunctival papillae, superficial punctate keratitis
and marked chemosis are almost always present. Subconjunctival hemorrhage (hemorrhagic conjunctivitis),
pseudomembrane or true membrane formation and preauricular lymph nodes are usually present. In chronic,
recalcitrant or severe cases, peripheral subepithelial corneal infiltrates may occur, leading to marginal ulceration
with anterior uveitis.
PATHOPHYSIOLOGY
Chlamydia trachomatis is an intracellular parasite that contains its own DNA and RNA. The sub-group A causes
chlamydial infections, the serotypes A, B, Ba and C cause trachoma, and serotypes D through K produce adult
inclusion conjunctivitis. The mode of ocular transmission may be hand contact from a site of genital infection to
the eye, laboratory accidents, a mother infecting the newborn, shared cosmetics and occasionally an improperly
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chlorinated hot tub.
Diagnostic testing for chlamydia is expensive and difficult to interpret. The preferred method of identification is
to culture the organism. Conjunctival scrapings for Giemsa staining will show intracytoplasmic inclusion bodies
in epithelial cells, polymorphonuclear leukocytes and lymphocytes.
The infectious organism in gonococcal conjunctivitis is Neisseria gonorrhoeae, a gram-negative, intracellular
diplococcus capable of invading an intact mucosal membrane. Transmission is generally by direct or indirect
sexual contact or contact with an infected individual. N. gonorrhoeae’s ability to penetrate an intact corneal
epithelium makes the risk of corneal infection and ulceration high.
MANAGEMENT
In treating chlamydial conjunctivitis, many doctors consider oral tetracycline 250 to 500mg q.i.d. for three
weeks the treatment of first choice. But since tetracycline must be administered one hour before or after meals to
avoid gastrointestinal side effects and interference of dairy products with its efficacy, other oral medications
may be more appropriate. Amoxacillin and erythromycin 250 to 500mg q.i.d. for three weeks or doxycycline
100mg b.i.d. for one week are acceptable alternatives.
Currently, the drug of choice is azithromycin (Zithromax). Taken as a 1 gram dose, by mouth, one time, it has
been documented as being as effective for the treatment of genital chlamydial infection as doxycycline. Topical
therapy is adjunctive and includes erythromicin, tetracycline or sulfacetamide t.i.d. for three weeks as well.
Patients with gonococcal conjunctivitis require immediate conjunctival scrapings for culture and sensitivity
testing. Medical management of gonococcal infection begins with an intramuscular loading dose of ceftriaxone
1g. Ideally, the patient should be hospitalized and given one gram of ceftriaxone intravenously within 12 to 24
hours. Following discharge, resume treatment with either erythromicin 250 to 500mg p.o. q.i.d., tetracycline 250
to 500mg p.o. q.i.d. or doxycycline 100mg p.o. b.i.d.
Begin ocular management with saline lavage to clear the mucopurulent debris from the lids and conjunctiva. A
topical fluoroquinolone (ofloxacin or ciprofloxacin) is appropriate if corneal infection occurs. However, because
gonococcal conjunctivitis does not respond to topical antibiotics, topical therapy is usually not indicated.
CLINICAL PEARLS
●
Inclusion conjunctivitis should be one of the differential diagnoses any time a patient presents with a
chief complaint of chronically red eyes or follicular conjunctivitis that is recalcitrant to topical therapies.
Follow up should be weekly. Educate patients that the disease is contagious and that partners are at risk
and should be examined.
●
Follow up with gonococcal conjunctivitis patients every day until you see consistent improvement.
Educate the patients regarding the circumstances surrounding the disease and that partners at risk should
be informed about the possibility of infection. Finally, contact the Centers for Disease Control for
instructions and recommendations.
Other reports in this section
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Handbook of Ocular Disease Management - Conjunctival Neoplasms
Conjunctival Neoplasms
Signs and symptoms: The primary conjunctival neoplasms
seen in optometric practice include squamous cell carcinoma
and, to a much lesser extent, malignant melanoma. With both
these conditions, the typical patient tends to be older (50-plus)
fig01.jpg (5755 bytes)
and white, often with a significant history of chronic sun
exposure. Systemic immunocompromise may also predispose
some patients to develop these neoplasms.
Squamous cell carcinoma of the conjunctiva often shows rapid
Two views of conjunctival neoplasm
onset and progression. In the early
in squamous cell carcinoma.
stages, there may merely be a mild dysplasia, which often
resembles a pinguecula, pterygium or even a phlyctenule. As the
lesion grows, an elevated, fleshy mass of pink tissue develops in
the interpalpebral space. Most often the lesion abuts the corneal
limbus. These irregularly shaped neoplasms develop a rich
intrinsic blood supply from the surrounding conjunctiva and
episclera, with large-diameter "feeder vessels" emanating from
the mass. Another hallmark sign is the presence of overlying
"flaky" placoid white areas on the tumor surface, referred to as
leukoplakia; this is a common finding in advanced or invasive
conjunctival squamous cell carcinoma.
Conjunctival melanomas are relatively rare, accounting for fewer than 2% of all ocular malignancies.
These lesions may present as a flat or nodular pigmented area, although amelanotic conjunctival
melanomas have been documented. Like squamous cell carcinoma, they typically develop at the
limbal margin. Vascularization is again readily evident, with numerous feeder vessels supplying the
lesion. Unlike carcinomas, however, conjunctival melanomas tend to become multicentric if not
diagnosed and managed promptly. Often, two or more focal neoplasms will "sprout" from a common
feeder vessel, much like strawberries on a vine. Melanomas tend to progress more rapidly, and are
more invasive into underlying ocular tissues. So, it is not uncommon to see associated uveitis or
secondary glaucoma if the lesion invades the anterior chamber.
Conjunctival neoplasms may merely pose a cosmetic concern for patients in the early stages, and
they may be noted on routine ocular examination. Larger lesions may interfere with lid function,
causing dry eye complaints and possibly dellen formation on the adjacent cornea. Advanced, invasive
lesions may compromise the episclera, sclera, cornea or angle structures. Pain may be a significant
factor in later stages due to associated keratitis, uveitis or rise in intraocular pressure.
Pathophysiology: Neoplastic disorders can affect virtually all ocular tissues. Squamous cell
carcinoma and melanoma of the conjunctiva represent primary malignancies of ectodermal tissue;
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they are forms of skin cancer. There are many risk factors for skin cancer, but for these lesions the
most significant cause by far is chronic exposure to ultraviolet radiation. At the cellular level, these
malignancies represent tissue that no longer responds to its genetic "program"; cells divide at an
accelerated rate, invading and destroying surrounding tissue through compression and competition
for blood supply. Malignancies lose the ability to carry out the normal metabolic functions of their
tissue of origin, further compromising the organ system.
Management: Because the conjunctiva is only loosely adherent to underlying ocular tissues, the
prognosis for conjunctival neoplasms is generally very good. There is a relatively small risk of local
extension into the eye and an even smaller risk of metastasis, provided the lesions are detected and
treated early.
Biopsy is always indicated for unusual or suspicious lesions on the bulbar or palpebral conjunctiva.
Biopsy-proven lesions call for surgical excision of the involved conjunctival tissue. The excision
involves taking wide margins so that all of the visible tumor mass is removed. Typically, the surgeon
then applies cryo- or laser therapy to the remaining borders to ensure complete destruction. In
advanced cases in which the tumor extends into the surrounding tissues, enucleation or even
exenteration of the orbit may be required to preserve the patient's life.
Alternative therapy for those who cannot or will not undergo surgery for these neoplasms includes
chemotherapy or local radiation therapy. Chemotherapy does not enjoy a high success rate in cases
of conjunctival neoplasm, and may induce a significant array of unpleasant side effects. Radiation of
these lesions is also less successful than local excision, and poses great risk to surrounding ocular
tissues at high doses. Corneal burns and radiation retinopathy are potential complications of this
treatment.
Clinical Pearls:
●
Suspect neoplasms with any rapidly growing mass on the conjunctival surface that fails to
respond to antibiotic or anti-inflammatory therapies. Realize that two or more feeder vessels,
leukoplakia, changes or variations in color or a predilection toward bleeding all constitute "red
flags" for malignancy.
●
When you suspect malignant melanoma of the conjunctiva, evert both the upper and lower lids
to inspect for additional lesions of the palpebral conjunctiva. Likewise, always perform a dilated
fundus examination and consider gonioscopy to rule out extension into the uvea.
●
While most conjunctival neoplasms carry a good prognosis, metastasis is always a possibility;
this is particularly true with melanoma, which can be extremely aggressive. Comanage
patients with an experienced oncologist to be certain that the cancer has not spread to other
organ systems. Because the liver is the single most common site of metastasis from ocular
malignancies, testing liver enzymes is an important consideration for any patient with cancer of
the eye.
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Other reports in this section
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CONJUNCTIVAL LYMPHOMA
Signs and Symptoms
Conjunctival lymphomas represent a mass lesion of the
superficial ocular surface. They are classically described as
"salmon-colored patches," and may present bilaterally in as many
as 20% of patients. The lesions are fleshy and may grow rapidly.
Often, they appear to arise from within the fornix and extend
toward the cornea. Despite the characteristic appearance,
conjunctival lymph-omas resemble several other benign tumors
of the ocular surface, including squamous papilloma, pyogenic
granuloma and lymphangiectasis. Patients with conjunctival
lymphoma tend to be young to middle-aged adults. They may
complain of chronic redness but rarely report ocular discomfort.
Pathophysiology
Malignant lymphoma.
Lymphoma is best described as malignant growth of lymphoid tissue, or cancer of elements of the
lymphatic system. Lymphoid tissue is present in most organs throughout the body, and is connected
by channels and conduits to lymph nodes, located primarily in the neck, axillae, groin and abdomen.
In the eye, lymphoma manifests as a conjunctival or orbital mass, a choroidal infiltration with
secondary uveitis, or an infiltrative optic neuropathy.
A variety of nomenclature is used to describe lymphoid tumors of the conjunctiva. Some sources
divide the lesions into three classifications: (1) benign reactive lymphoid hyperplasia; (2) atypical
lymphoid hyperplasia; and (3) malignant lymphoma. Benign lymphoid hyperplasia contains mature
follicles composed of B-cell lymphoblasts surrounded by a mantle zone of mature T cells.1 Atypical
lymphoid hyperplasia may represent an evolving lymphoma, containing "burned-out" or "abortive"
follicles. Malignant lymphomas may be further subdivided into: (1) MALT, or mucosa- associated
lymphoid tissue lymphoma (sometimes called a "MALToma"); and (2) non-MALT lymphoma. MALT
lymphomas are portrayed as being less aggressive, while non-MALT lesions are considered highly
malignant and invasive. The majority of conjunctival lymph-omas are monoclonal proliferations of B
lymphocytes.2 Lymph-oid tumors of the conjunctiva are associated with systemic lymphoma in about
31% of patients.3
Management
Biopsy is crucial in any case of suspicious conjunctival
lesions. The most critical element, after establishing the
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presence of a conjunctival lymphoma, is differentiating
between the MALT and non-MALT varieties. In addition,
any patient with biopsy-proven lymph-oma deserves a
complete medical evaluation to determine if systemic
lymphoma is present. This includes basic hematology
(CBC with differential) as well as examination by a
hematologist and/or oncologist. Radiographic imaging of
the head, chest and abdomen are usually also obtained
if systemic involvement is suspected.
Therapy for conjunctival lymphoma depends on the
More extensive lesion.
disposition of the tumor and whether there is
disseminated lymphoma elsewhere in the body. Isolated conjunctival lymphoma (i.e., involving the
conjunctiva but no other ocular or systemic structures) is most often treated with external beam
irradiation. Dosage and exposure tends to be higher for more aggressive non-MALT lymphomas,
though care must be taken to minimize long-term complications of ocular radiation such as
xerophthalmia or cataract formation.4 Recent studies have shown that intralesional interferon may
also be a viable form of therapy for MALT lymphomas of the conjunctiva.5,6
Clinical Pearls
●
Though conjunctival lymph-oma may be associated with systemic lymphoma, the ocular
lesions have not been shown to metastasize to any significant degree. The five-year survival
rate for MALT lymphomas is excellent and reported to be 93%.7
●
Localized therapy for conjunctival lymphoma may not be required in individuals with
disseminated lymphoma undergoing systemic chemotherapy.
1. Grossniklaus HE, Yanoff M. Orbit. In: Tasman W, Jaeger EA, eds. Duane's Ophthalmology, 1998 CD-ROM
Edition. Hagerstown, MD: Lippincott-Raven Publishers, 1998.
2. Jakobiec FA, Knowles DM. An overview of ocular adnexal lymphoid tumors. Trans Am Ophthalmol Soc
1989; 88:420-42; discussion 442-4.
3. Shields CL, Shields JA, Carvalho C, et al. Conjunctival lymphoid tumors: clinical analysis of 117 cases and
relationship to systemic lymphoma. Ophthalmology 2001; 108(5):979-84.
4. Bessell EM, Henk JM, Whitelocke RA, et al. Ocular morbidity after radiotherapy of orbital and conjunctival
lymphoma. Eye 1987; 1 (Pt 1):90-6.
5. Zinzani PL, Magagnoli M, Ascani S, et al. Nongastrointestinal mucosa-associated lymphoid tissue (MALT)
lymphomas: clinical and therapeutic features of 24 localized patients. Ann Oncology 1997; 8(9):883-6.
6. Blasi MA, Gherlinzoni F, Calvisi G, et al. Local chemotherapy with interferon-alpha for conjunctival mucosa-
associated lymphoid tissue lymphoma: a preliminary report. Ophthalmology 2001; 108(3):559-62.
7. Zucca E, Conconi A, Roggero E, et al. Non-gastric MALT lymphomas: a survey of 369 European patients.
The International Extranodal Lymphoma Study Group. Ann Oncol 2000;11, Suppl 4:99.
Other reports in this section
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Handbook of Ocular Disease Management - Bacterial Keratitis
Bacterial Keratitis
Signs and Symptoms: The patient with bacterial keratitis will
generally present with a unilateral, acutely painful, photophobic,
intensely injected eye. Visual acuity is usually reduced, and
profuse tearing is common. There will be a focal stromal infiltrate
with an overlying area of epithelial excavation.
fig01.jpg (5755 bytes)
Mucopurulent discharge may emanate from the lesion. The
cornea may be edematous. The conjunc tival and episcleral
vessels will be deeply engorged and inflamed, often greatly out of
Bacterial keratitis.
proportion to the size of the corneal defect. A pronounced
anterior chamber reaction, often with hypopyon, is present in severe cases. Intraocular pressure may
be low due to secretory hypotony of the ciliary body, but often will be elevated due to blockage of the
trabecular meshwork by the inflammatory cells. Often, the eyelids will also be edematous.
Pathophysiology: Once the corneal defenses are breached, specifically the corneal glycocalyx, the
cornea is prone to infection by pathogenic bacteria. Precipitating factors to corneal defense
breakdown include direct corneal trauma, chronic eyelid disease, tear film abnormalities affecting the
ocular surface and hypoxic trauma from contact lens wear.
Pathogenic bacteria colonize the corneal stroma and immediately become antigenic, both directly and
indirectly, by releasing enzymes and toxins. This sets up an antigen-antibody immune reaction with
chemotactic factors inducing an inflammatory reaction. The body mobilizes polymorphonuclear
leukocytes (PMN) which aggregate at the area of infection, creating an infiltrate. The PMNs
phagocytize and digest the bacteria and damage stromal tissue utilizing numerous enzymes that tend
to leak from the PMN into the stroma.
The collagen stroma is poorly tolerant of the bacterial and leukocytic enzymes and undergoes
degradation, necrosis and thinning. This results in scarring of the cornea. With severe thinning, the
cornea may perforate, thus introducing bacteria into the eye with ensuing endophthalmitis.
The most commonly occurring organisms in bacterial keratitis vary depending on the precipitating
factors of the ulcer and the geographic location of the patient. In cases involving contact lens wear
and cosmetic mascara, the most common infective organism is Pseudomonas aeruginosa. Overall
throughout North America, the most common infective organism in bacterial keratitis is
Staphylococcus aureus.
Management: Proper diagnosis and prompt therapy are essential to preserve vision in bacterial
keratitis. Your first step in management should be to obtain corneal scrapings for microbiologic
studies. The standard of care is to obtain a platinum spatula and plate onto blood-chocolate agar
medium. However, the effectivity of the fluoroquinolones has led many practitioners away from this
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Handbook of Ocular Disease Management - Bacterial Keratitis
standard. Identification, as well as sensitivity studies, will aid in management. An alternative for
treatment of less severe keratitis is a mini-tip Culturette. Scrape the lesion with the Culturette, then
place it in the media-containing carrier. The sensitivity of this approach compared to platinum spatula
collection and plating was 83.3% sensitivity and 100% specificity.
With the advent of fluoroquinolone antibiotics, many clinicians have dropped culturing as part of the
diagnostic regimen. However, we recommend you still obtain cultures for central lesions that threaten
vision, are at risk of perforation, and in patients in institutions such as nursing homes and hospitals
where methicillin-resistant Staph. aureus infections are possible.
Even if the patient has been cultured, you must initiate broad-spectrum, empirical antibiotic therapy
prior to receiving the results. A popular initial therapy is the fluoroquinolone Ciloxan (ciprofloxacin ,
Alcon), two drops every 15 minutes for six hours, followed by two drops every 30 minutes for 18
hours, and then tapered depending on patient response. Another fluoroquinolone, Ocuflox (ofloxacin,
Allergan) is also an effective treatment for bacterial keratitis. Both fluoroquinolones have been proven
to be as effective at managing bacterial keratitis as the previously used fortified antibiotics, but with
significantly fewer side effects. Newer fourth-generation fluoroquinolones promise to have similar
efficacy against gram-negative pathogens and broader activity against gram-positive species.
Strong cycloplegia is also mandatory in order to increase patient comfort and minimize inflammation.
The weakest cycloplegic that you should use is scopolamine 0.25% tid. If this is insufficient, then
prescribe atropine 1% bid. Adjunctive use of cold compresses will also help to reduce inflammation.
If there is evidence of secondary inflammatory glaucoma occurring, then a topical aqueous
suppressant agent may be indicated. Follow the patient frequently until the infection is well controlled.
If the results of cultures and sensitivities show that the antibiotic you chose initially was appropriate
for the infective organism, or if the patient shows signs of clinical improvement (or the ulcer does not
worsen and pain and photophobia are reduced) at the 24-48 hour follow up visit, then add a topical
corticosteroid such as Pred Forte (prednisolone, Allergan) or Lotemax (loteprednol, Bausch & Lomb)
q2h. Follow the patient every 24 hours, and taper the medications as the condition improves.
Clinical Pearls:
●
If a patient presents with a corneal infiltrate without overlying epithelial staining, then the
condition may not be infectious bacterial keratitis.
●
The use of strong bacteriocidal antibiotics will eliminate the infective organisms and sterilize
the ulcer, but will do nothing to quell the inflammatory reaction. In this instance, the
inflammatory reaction is as damaging to the cornea as is the infective organism. If there is
evidence that the antibiotic is suppressing the infective organism, then corticosteroid use will
inhibit the inflammatory reaction and speed healing and reduce corneal scarring.
●
For steroids to be most beneficial, prescribe them while the ulcer bed is still open, usually
within the first 24-48 hours after you initiate antibiotic therapy. If you wait until the ulcer re-
epithelializes before adding a steroid, their beneficial effects will be reduced. A cautionary
note: Be comfortable that the antibiotic has sterilized the ulcer before instituting the steroid.
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Handbook of Ocular Disease Management - Bacterial Keratitis
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Bacterial Keratitis
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Handbook of Ocular Disease Management - Fungal Keratitis
Fungal Keratitis
Signs and Symptoms: Fungal keratitis shows no predilection
for age, gender or race, although those with compromised
immunity are especially prone. Risk factors include ocular
trauma--particularly if organic vegetative matter is involved--
topical steroid therapy and preexisting ocular or systemic
immunosuppressive diseases. Those who work with plants may
be at greater risk. Fungal infections are also more common in
tropical environments. An altered epithelial barrier increases the
threat. Pain is typically severe at first, but may diminish later as
Fungal keratitis.
the corneal nerves become damaged.
In the cornea, filamentary fungal infections initially produce a feathery, branching pattern. The cornea
takes on a dull gray appearance with possible heaping of epithelium and a dry, rough texture.
Typically a severe anterior uveitis and plasmoid aqueous with hypopyon appears. The characteristic
corneal appearance disappears later on as the fungal keratitis begins to resemble advanced bacterial
keratitis. Misdiagnosis at this point is likely. Yeast infections, however, remain localized, with a "button
appearance," an expanding stromal infiltrate and a relatively small epithelial ulceration.
Pathophysiology: There are two types of fungi, molds and yeasts. Molds (filamentary fungi) are
further subdivided into septate (the most common causes of fungal keratitis) and non-septate
organisms. They produce feathery colonies that join together to produce hyphae. Yeasts, however,
form pseudohyphae. The non-septate filamentary fungi are responsible for orbital disease, but rarely
infect the cornea. Of all possible fungal infections of the cornea, the vast majority is caused by
Fusarium, Aspergillus (both filamentary fungi) and Candida (a yeast).
Organic trauma is the major cause of filamentary
The Fluoroquinolone Advantage
fungal keratitis. Immunosuppression or a
chronically compromised epithelial barrier
usually causes yeast infection. A disrupted
corneal defense system can allow for Candida
infection, opportunistic yeast that is part of the
normal human flora. Once fungi have colonized
the stroma, they penetrate into the deeper layers
and are inaccessible to diagnostic and
therapeutic measures. The organisms' large size
precludes complete ingestion by inflammatory
cells from the host's immune response.
Management: Diagnosis of fungal keratitis
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Handbook of Ocular Disease Management - Fungal Keratitis
The fluorinated quinolones—Ciloxan
begins with clinical suspicion; either culture or
(ciprofloxacin, Alcon Laboratories), Ocuflox
corneal biopsy confirms it. Diagnosis typically
(ofloxacin, Allergan), Quixin (levofloxacin,
occurs late, as many frequently misdiagnose
Santen) and Chibroxin (norfloxacin, Merck)--have
fungal keratitis as bacterial keratitis. Clinicians
revolutionized the standard of care for cases of
often consider fungal keratitis only after a
infection or increased risk of infection of the
presumed bacterial keratitis worsens during
conjunctiva, cornea, anterior segment and
antibiotic therapy.
posterior segment.
The standard corneal scraping performed in
More potent and effective "off of the shelf" than
bacterial keratitis is acceptable; however, in
previous antibiotics, they have all but eliminated
addition to regular cultures with blood and
the need for fortified compounds in treating
chocolate agar incubated at 370° C for bacteria,
moderate to severe infections, reducing expense,
inoculate additional blood and Sabouraud agar
error and the risk of contamination during
plates at room temperature. Anti-fungal
sensitivity testing is unreliable and correlates
preparation.
poorly with clinical efficacy. Reserve corneal
biopsy for cases where you suspect fungal infection yet cultures are negative, or in cases where
ulceration persists despite aggressive antimicrobial therapy.
Treating fungal keratitis is difficult. Most antifungal medications are merely fungistatic, and require an
intact immune system and prolonged therapeutic course. Except for Natacyn (natamycin 5%, Alcon),
all antifungal medications must be adapted for ophthalmic use from systemic drugs. The result:
considerable ophthalmic toxicity.
Drug classes used to treat fungal keratitis include the polyene antibiotics (nystatin, amphotericin B,
natamycin); pyrimidine analogs (flucytosine); imidazoles (clortrimazole, miconozole, ketoconazole);
triazoles (fluconazole, itraconazole); and silver sulfadiazine. Steroids are contraindicated; they will
exacerbate the disease. For filamentary fungal infections, topical Natacyn is the first choice.
Alternatives include amphotericin B 0.15% and flucytosine 1% 150 mg/kg--the same therapy for yeast
infections. An alternative treatment in yeast infections is fluconazole 0.5% 200 mg and miconozole
1%. All therapies are indicated hourly around the clock.
Clinical Pearls:
●
It is practically impossible to differentiate bacterial keratitis from fungal keratitis on clinical
judgment alone, especially in advanced cases.
●
A history of injury with vegetative matter is not necessary for a patient to develop fungal
keratitis. Remember the strong role of immunosuppression in the development of Candida
infections.
●
In our combined experience, we have only once seen a case where a patient who actually
underwent ocular trauma from vegetative matter progressed to fungal keratitis. We do not
recommended that a patient receive prophylactic antifungal therapy in these instances.
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Handbook of Ocular Disease Management - Fungal Keratitis
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Handbook of Ocular Disease Management - Acanthamoeba Keratitis
Acanthamoeba Keratitis
Signs and Symptoms: Acanthamoeba keratitis can occur in
patients of any age, sex or race, but mostly manifests in young,
healthy adults. The list of risk factors is long: corneal foreign
body, contact with non-sterile water, bullous keratopathy,
fig01.jpg (5755 bytes)
neurotrophic keratopathy, herpes simplex keratitis, radial
keratotomy, swimming and scuba diving, basement membrane
dystrophy, contact lens wear and bacterial keratitis. Cases
sometimes arise with no identifiable risk factors. Essentially, any
event that disrupts the corneal epithelium is a potential risk factor
Acanthamoeba keratitis.
for Acanthamoeba keratitis.
Patients with Acanthamoeba keratitis typically present with a unilateral, red, painful eye. Initially, there
is typically a non-specific epitheliopathy which can progress to ulceration with infiltration. Limbititis
occurs as the initial finding in 94% of early stage cases and in 84% of late-stage cases.1-3 Another
common finding is radial keratoneuritis, or perineuritis; this involves irregularly thickened corneal
nerves in the anterior to mid-stroma with shaggy borders. Other clinical signs of Acanthamoeba
keratitis include irregular epithelial defect, corneal microcysts, punctate keratopathy, bullous
keratopathy, disciform stromal keratitis, pseudodendritic keratitis, anterior uveitis and a
granulomatous stromal reaction. While Acanthamoeba keratitis has historically been associated with
stromal ring infiltrate formation, only 6% of early cases and 16% of late cases actually present in this
manner clinically.1-3
About half of patients report significant pain, the rest experience only mild irritation and foreign-body
sensation.4,5 Those who do report pain often present a degree much worse than the clinical
appearance suggests. Rarely is Acanthamoeba keratitis correctly diagnosed in the early stage. It
typically follows a chronic course that waxes and wanes over weeks to months and never fully heals
despite seemingly appropriate therapy. In fact, the diagnosis is often finally made when all other
treatments fail.
Pathophysiology: Acanthamoeba keratitis occurs from Acanthamoeba castellani, an opportunistic
free-living soil amoeba that is most commonly associated with incorrect contact lens handling and
exposure to unsanitary conditions. While rare, the incidence of recognized Acanthamoeba keratitis is
rising, due mostly to correct diagnoses in cases of non-specific keratitis as well as increased use of
confocal microscopy. This noninvasive diagnostic modality readily identifies Acanthamoeba cysts in
the cornea. Unortunately, this technology is not widely available.
As we said previously, few correctly diagnose Acanthamoeba keratitis early on. Clinicians have
mistaken Acanthamoeba keratitis for herpetic, fungal and bacterial keratitis. Acanthamoeba keratitis is
partially amenable to non-protozoan treatments, and can wax and wane for years before a correct
diagnosis is made. Certain antibiotics as well as preservatives in topical medications create a hostile
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Handbook of Ocular Disease Management - Acanthamoeba Keratitis
environment for the microbe; in response, Acanthamoeba will encyst and become dormant, reducing
the symptoms and clinical signs. So Acanthamoeba may seem partially responsive to other
treatments, assuming a chronic course prior to the correct diagnosis.
Acanthamoeba keratitis can present initially as a dendritic keratitis similar to herpes simplex keratitis
(HSK), with this exception: there are no herpetic terminal end bulbs in Acanthamoeba keratitis. There
probably have been cases of Acanthamoeba keratitis that clinicians have mistakenly treated for HSK.
And, there have been reports of coexistent infections of both HSK and Acanthamoeba keratitis, with
the Acanthamoeba presenting as a secondary, opportunistic infection. The Acanthamoeba organism
nestles in the thickened border of the epithelium. Consider Acanthamoeba infection in cases of
presumed or actual herpes simplex keratitis that does not respond to standard antiviral therapy.
Corneal scrapings of Acanthamoeba may be cultured for diagnosis. This calls for non-nutrient agar
with overlay of either Escherichia coli or Enterobacter. Culturing can take 1-9 days, sometimes longer.
Unfortunately, the diagnostic yield is low and cultures are often falsely negative. Cultures often will
reveal the presence of bacteria, because Acanthamoeba frequently coexists with bacterial colonies
upon which it feeds. Acanthamoeba often accompanies other corneal diseases, and may not be the
primary or most active disease process in a combined keratitis.
Management: Treatment of Acanthamoeba keratitis is difficult due to the organism's ability to encyst
with the use of topical medications. Effective medications include topical polyhexamethylene
biguanide (PHMB), propamidine isethionate (Brolene), chlorhexidine digluconate 0.02%, polymixin B,
neomycin and clortrimazole 1%. In one series of 10 patients, the combination of Brolene and PHMB
successfully cured all cases of Acanthamoeba keratitis. Cautious introduction of topical steroids along
with anti-amoebic therapy helped resolve the inflammation and provided symptomatic relief.
Clinical Pearls:
●
Strongly suspect Acanthamoeba keratitis in chronic keratitis that does not respond to
treatment.
●
While ring infiltration has historically been associated with Acanthamoeba keratitis, it is a
relatively rare finding and typically occurs late in the disease. Non-specific epitheliopathy is
typically the presenting feature.
●
As Acanthamoeba feeds upon bacteria, it frequently accompanies bacterial ocular infections.
●
Acanthamoeba play a part in coinfections, sometimes explaining why other corneal infections
do not respond to conventional therapy.
1. Bacon AS, Dart JK, Ficker LA, et al. Acanthamoeba keratitis. The value of early diagnosis.
Ophthalmology 1993 Aug;100(8):1238-43.
2. Bacon AS, Frazer DG, Dart JK, et al. A review of 72 consecutive cases of Acanthamoeba keratitis, 1984-
1992. Eye 1993;7 ( Pt 6):719-25.
3. Bernauer W, Duguid GI, Dart JK.Early clinical diagnosis of acanthamoeba keratitis. A study of 70 eyes.
Klin Monatsbl Augenheilkd 1996 May;208(5):282-284.
4.Tabin G, Taylor H, Snibson G,et al. Atypical presentation of Acanthamoeba keratitis.Cornea 2001 Oct;20
(7):757-9.
5. Roters S, Aisenbrey S, Severin M, et al. Painless acanthamoeba keratitis. Klin Monatsbl Augenheilkd
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Handbook of Ocular Disease Management - Acanthamoeba Keratitis
2001 Aug;218(8):570-3.
Other reports in this section
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Acanthamoeba Keratitis
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Handbook of Ocular Disease Management - Filamentary Keratitis
Filamentary Keratitis
Signs and Symptoms: Patients presenting with filamentary
keratitis generally report ocular discomfort ranging from mild
foreign-body sensation to severe pain. Variable tearing and
photophobia are likewise present. The condition may be
fig01.jpg (5755 bytes)
unilateral or bilateral, depending upon the underlying etiology.
Signs include ocular hyperemia particularly in the limbal area,
and possibly a pseudoptosis. The hallmark finding is the
presence of mucus filaments within the preocular tear film
Filamentary keratitis.
adhering to the corneal surface. These filaments are typically
tadpole-shaped (the "head" adheres firmly to the corneal epithelium, while the "tail" floats freely within
the tear film). Rose bengal or lissamine green dye makes the filaments more readily visible on
biomicroscopy. Other findings may include a reduced fluorescein tear break-up time and a punctate
epithelial keratopathy.
Many patients with filamentary keratitis have underlying systemic conditions, particularly connective
tissue disorders. The condition may be more common in women and the elderly. Patients with
immune deficiencies also are at greater risk.
Pathophysiology: Filamentary keratitis most often accompanies keratoconjunctivitis sicca. Mucous
filaments form when the normally soluble mucin component of the tear film becomes corrupted,
causing it to precipitate out as particles or strands. Loose, compromised epithelial cells bind with
these mucin strands, forming long filaments that adhere to damaged sites on the corneal surface. As
the lids open and close with each blink, they tug at the loose end of the filaments, stimulating the pain-
sensitive corneal nerves.
Other conditions that can induce a filamentary keratitis include superior limbic keratoconjunctivitis
(SLK) of Theodore, prolonged patching following cataract or other ocular surgery, epitheliopathy due
to aerosol or radiation keratitis, herpetic keratitis (both simplex and zoster), recurrent corneal erosion,
neurotrophic keratitis, bullous keratopathy, and systemic disorders, including diabetes and psoriasis.
Management: Treatment for filamentary keratitis involves eliminating the mucus filaments as
thoroughly as possible and addressing the underlying cause. In most cases, management begins with
physical removal of the filaments at the slit lamp, using a jeweler's forceps under topical anesthesia.
Copious lubrication therapy with artificial tears (preferably non-preserved) helps address the ocular
discomfort and rejuvenate the precorneal tear film. Punctal occlusion therapy may help in persistent
cases of dry eye.
In more severe cases of filamentary
keratitis, pharmaceuticals may help to
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Handbook of Ocular Disease Management - Filamentary Keratitis
eliminate the filaments and improve
Antibiotics, Steroids and Combination Medications
patient comfort. N-acetylcysteine
The anterior eye's limited response to a broad variety of
(Mucomyst) is a mucolytic agent used
insults sometimes makes it difficult to differentiate viral,
primarily as an inhalant for patients with
bacterial or allergic causes. Using combination medicines
bronchial disease such as emphysema,
such as Tobradex (tobramycin and dexamethasone,
pneumonia or cystic fibrosis. In its
Alcon) or Maxitrol (neomycin, polymixin B and
topical form (2-10%), acetylcysteine
dexamethasone, Alcon), is often effective because the
effectively dissolves corneal filaments.
medications can simultaneously quiet infection and
While not commercially available in the
inflammation.
United States, you can readily obtain
acetylcysteine from a compounding
Unfortunately, this approach can also produce
pharmacist.
complications. Inappropriately prescribed topical steriods
can cause herpes simplex epithelial infection to accelerate
Manage more severe forms of
out of control. In patients with microbial keratitis,
filamentary keratitis with a high-water
increased ulceration and even corneal perforation may
(~70%), soft bandage contact lens with
ensue if the organism is resistant to the antibiotic. Steroids
prophylactic antibiotic drops bid-tid. Be
can also impede healing and cause corneal melting. And
prepared to manage this condition for
in cases where only a steroid is needed, the additional
prolonged periods. Filamentary keratitis
antimicrobial agents may actually produce toxicity.
may take weeks or even months to
resolve, depending on the etiology and the aggressiveness of therapy. Even after the filaments
dissipate, the underlying disease must be controlled or recurrences are likely.
Clinical Pearls:
●
Remember that filamentary keratitis is not a disease per se, but rather a sign of a severe
ocular surface disorder. Always determine the root cause of this condition before initiating
therapy.
●
Inform patients that prolonged therapy may be necessary to alleviate this condition, which is
often chronic. Antibiotic solutions do not help as a primary therapy for filamentary keratitis,
although they may provide prophylaxis on compromised corneas. Topical corticosteroids or
NSAIDs may palliate the associated discomfort, depending on the underlying etiology.
●
N-acetylcysteine 5% solution is often available from a compounding pharmacy, and is often
helpful in managing filamentary keratitis. Advise patients that this solution may smell like rotten
eggs, and can also be quite expensive for a relatively small amount. If formulated without
preservatives, the patient must discard it after about 30 days.
Other reports in this section
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Handbook of Ocular Disease Management - Filamentary Keratitis
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Filamentary Keratitis
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Handbook of Ocular Disease Management - Scleritis
Scleritis
SIGNS AND SYMPTOMS
Unlike the mild sensitivity of episcleritis, true scleritis presents with
severe, boring ocular pain which may also involve the adjacent head
and facial regions. The scleral vessels are significantly dilated, as are
the overlying vessels of the episclera and bulbar conjunctiva. The
affected eye may be so injected in some cases that the eye actually
takes on a deep red, almost purple, hue. This presentation may be
sectoral or diffuse.
Patients typically report a gradual onset of the pain and redness, with associated photophobia, tearing and
decreased vision. Slip lamp evaluation may reveal scleral nodules (nodular scleritis), peripheral keratitis and
secondary uveitis in some instances. In severe cases of necrotizing scleritis, the sclera may become transparent
due to chronic inflammation, revealing the underlying dark blue of the choroid.
PATHOPHYSIOLOGY
Scleritis is a primary inflammation of the sclera, which is often (over 50 percent of cases) associated with
systemic disease. Among the most common related disorders are rheumatoid arthritis, ankylosing spondylitis,
systemic lupus erythematosus, polyarteritis nodosa, Wegener's granulomatosis, herpes zoster virus, gout and
syphilis.
Unlike episcleritis, the inflammation characteristic of scleritis has the capacity to spread to other ocular tissues
of the anterior segment and/or posterior segment. Consequently, if you do not begin treatment of scleritis
immediately, the condition poses the risk of severe visual compromise in the form of cataracts, secondary
glaucoma, choroidal or exudative retinal detachment or optic atrophy.
MANAGEMENT
Topical medications alone are generally insufficient in managing scleritis. In addition to cycloplegia
(scopolamine 0.25% BID/QID or atropine 1% BID) and a topical steroid, scleritis indicates a systemic anti-
inflammatory agents as well. Treat moderate sectoral or diffuse anterior scleritis with oral NSAIDs (e.g.,
ibuprofen 600mg QID or indomethacin 25mg TID).
If the inflammation is severe or necrotizing, or if non-steroidals alone fail to suppress the inflammation, use a
systemic steroid such as oral prednisone 80mg QD for two to three days, then slowly taper to 10 to 20mg daily.
It may also be necessary for patients to receive a small maintenance dose for up to one month to control the
condition. In rare cases, the patient may require immunosuppressive agents and should be managed by a
rheumatologist.
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Handbook of Ocular Disease Management - Scleritis
CLINICAL PEARLS
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Treated improperly, scleritis can render a great deal of damage to the affected eye.
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Be sure to distinguish between this disorder and the less threatening episcleritis.
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Occasionally, an atypical presentation of necrotizing scleritis without inflammation may occur; this is
known as scleromalacia perforans. In this presentation, the sclera thins significantly in discrete areas,
allowing for local outpouchings of the underlying choroid. There is no recognized treatment for this
condition.
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In all cases of scleritis, always consider the underlying cause to be systemic disease until proven
otherwise. Refer patients for a comprehensive medical evaluation, including serology and radiology
studies where appropriate. Specific tests may include: complete blood count (CBC) with differential,
erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), HLA-B27, rheumatoid factor (RF),
angiotensin-converting enzyme (ACE), fluorescent treponemal antibody absorption (FTA-ABS), lyme
titer, chest X-ray and sacroiliac joint films.
Other reports in this section
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Handbook of Ocular Disease Management - Episcleritis
Episcleritis
SIGNS AND SYMPTOMS
Episcleritis presents as a relatively asymptomatic acute onset redness
in one or both eyes. Typically, you'll observe a sectoral injection of the
episcleral and overlying conjunctival vessels, although the redness
may be diffuse throughout these tissues. Occasionally, there may be a
translucent white nodule centrally within the inflamed area (nodular
episcleritis). While some patients complain of mild pain or tenderness
to the affected region, particularly upon manipulation, often there is no
associated discomfort. The cornea remains clear in this condition,
although long-standing or recurrent episcleritis may lead to dellen
formation. There is no associated anterior chamber reaction.
PATHOPHYSIOLOGY
A benign inflammatory condition of the external eye, episcleritis is seen most commonly in young adults.
Women appear to be affected slightly more often than men. The disorder is idiopathic in the majority of cases,
however in certain instances there may be an association with some underlying systemic disease such as
rheumatoid arthritis, polyarteritis nodosa, systemic lupus erythematosus, inflammatory bowel disease,
sarcoidosis, Wegener's granulomatosis, gout, herpes zoster virus or syphilis.
MANAGEMENT
Most cases of episcleritis are self-limiting, meaning that they will resolve spontaneously within two to three
weeks even if the patient does not undergo treatment. However, patients who are experiencing discomfort may
benefit from a regimen of topical anti-inflammatory agents and lubricants.
Typically, prednisolone acetate 1% or fluorometholone acetate applied Q3-4H will speed resolution and
decrease the tenderness. The patient may use cold compresses and artificial tears liberally if discomfort persists.
More severe cases, particularly nodular episcleritis, may require oral NSAIDs to quell the inflammation.
Re-examine patients weekly. For those on topical steroid therapy for more than two weeks, perform tonometry
to monitor for elevation of IOP. Because of the association with systemic disorders, refer patients with
extremely severe presentations or more than three recurrences for a medical evaluation.
CLINICAL PEARLS
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Episcleritis is one of those conditions, like subconjunctival hemorrhage, that typically looks worse than
it is. Reassure patients that they do not have "pink-eye." However, be sure to distinguish this condition
from the more severe scleritis, which is far more painful and may have more serious implications.
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In severe or diffuse cases in which the differential diagnosis is more difficult, blanching the conjunctiva
and episclera with phenylephrine 2.5% will allow for better evaluation of the underlying sclera.
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When searching for the cause of episcleritis, remember that inflammatory bowel disease, ulcerative
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Handbook of Ocular Disease Management - Episcleritis
colitis, and Crohn's disease are the most commonly associated systemic disorders.
Other reports in this section
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Handbook of Ocular Disease Management - Pingueculitis
Pingueculitis
SIGNS AND SYMPTOMS
Pingueculae are characterized by yellowish, slightly raised,
interpalpebral lipid-like deposits in the nasal and temporal limbal
conjunctiva. They are found frequently in individuals who are
middle-aged and who experience chronic exposure to the sun. There
is no predilection for sex or race.
In most cases, pingueculae are an ancillary finding, causing little, if any, ocular symptoms. Frequently,
pingueculae can lead to the formation of pterygia. Both pingueculae and pterygia can become vascularized
and inflamed, and may be associated with corneal punctate epitheliopathy and corneal dellen (corneal
thinning secondary to dryness).
Pingueculitis occurs when a pinguecula becomes acutely inflamed, vascularized, red, irritated and highly
symptomatic.
PATHOPHYSIOLOGY
Pinguecula formation is typically seen in the older population and is considered by most researchers to be a
conjunctival degenerative processes initiated by exposure to noxious environmental stimuli and UV light.
The initial lesion is thought to result from chronic solar radiation, which alters the collagen and elastic
tissues of the conjunctival stroma and leads to elastotic degeneration and deposition of abnormal elastic
fibers in the conjunctival substantia propria.
Once a pinguecular elevation forms-depending on its size-the tear film may become thin and discontinuous
in that zone, producing a bed of dryness. When the lesion is inflamed, vascular dilation allows the release of
histamine, seratonin, bradykinin and prostaglandins, producing the acute irritation that characterize
pingueculitis. In severe cases the conjunctival surface becomes sufficiently dry to cause microulceration of
the conjunctival epithelium. When this occurs, the eye protects itself by attempting to cover the erosion,
leading to pterygium formation.
MANAGEMENT
Manage pinguecula based on symptomatology. For patients with occupations or hobbies that increase the
risk of pinguecula, counsel them on the preventative benefits of sunwear, UV-blocking coatings or goggles
that limit dust exposure.
In cases of mild pingueculitis, where symptoms are mild or when dellen are present, use ocular lubricating
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Handbook of Ocular Disease Management - Pingueculitis
drops such as Tears Naturale II or ointments such as Refresh PM or Lacrilube. When symptoms and
inflammation become significant, appropriate topical steroids, used Q2H to QID, include fluorometholone
0.25% (Flarex), 1% rimexolone acetate (Vexol), 0.12% prednisolone acetate suspension (Pred Mild), 0.12%
prednisolone sodium phosphate solution (Inflamase Mild), 1% prednisolone acetate suspension (Pred Forte)
1% prednisolone sodium phosphate solution (Inflamase Forte).
Consider surgical resection in severe cases where pterygia are present and are interfering with vision,
contact lens wear or corneal wetting.
CLINICAL PEARLS
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If you discover an intrapalpebral conjunctival mass or elevation, consider the differential
diagnosis. Lesions such as these are not all benign, and include conjunctival dermoid (a
white mass seen in Goldenhar's syndrome), cancerous or precancerous conjunctival
intraepithelial neoplasia (a unilateral, white, vascularized mass), phlyctenulosis (a white,
steep mass associated with Staphylococcus hypersensitivity and tuberculosis), pannus (a
fibrovascular conjunctival growth on the cornea associated with severe dry eye, chlamydial
infection, chemical or thermal injury), conjunctival retention cyst (a clear, fluid-filled sac)
and limbal follicle.
Other reports in this section
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Handbook of Ocular Disease Management - Pterygium
Pterygium
SIGNS AND SYMPTOMS
In most cases, routine ocular evaluation reveals pterygia in asymptomatic individuals or in patients who present
with cosmetic concern about a tissue "growing over the eye." In some instances, the vascularized pterygium may
become red and inflamed, motivating the patient to seek immediate care. In other cases, the irregular ocular
surface can interfere with the stability of the precorneal tear film, creating a symptomatic dry eye syndrome.
Rarely, the pterygium may induce irregular corneal warpage, or even obscure the visual axis of the eye, resulting
in diminished acuity.
Clinical inspection of pterygia reveals a raised, whitish, triangular wedge of fibrovascular tissue, whose base lies
within the interpalpebral conjunctiva and whose apex encroaches the cornea. The leading edge of this tissue
often displays a fine, reddish-brown iron deposition line (Stocker's line).
The vast majority of pterygia (about 90 percent) are located nasally. These lesions are more commonly
encountered in warm, dry climates, or in patients who are chronically exposed to outdoor elements or smoky/
dusty environments.
Pterygia must be distinguished from pingueculae, which are more yellow in color and lie within the
interpalpebral space but generally do not encroach beyond the limbus. Pingueculae also lack the wing-shaped
appearance of pterygia, the former being more oval or ameboid in appearance.
PATHOPHYSIOLOGY
Ultraviolet light exposure (both UV-A and UV-B) appears to be the most significant factor in the development
of pterygia. This may explain why the incidence is vastly greater in populations near the equator and in persons
who spend a great deal of time outdoors. Other agents that may contribute to the formation of pterygia include
allergens, noxious chemicals and irritants (e.g., wind, dirt, dust, air pollution). Heredity may also be a factor.
Whatever the etiology, pterygia represent a degeneration of the conjunctival stroma with replacement by
thickened, tortuous elastotic fibers. Activated fibroblasts in the leading edge of the pterygium invade and
fragment Bowman's layer as well as a variable amount of the superficial corneal stroma. Histologically,
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Handbook of Ocular Disease Management - Pterygium
pterygium development resembles actinic degeneration of the skin.
Pterygia often persist after surgical removal; these lesions appear as a fibrovascular scar arising from the
excision site. These "recurrent pterygia" probably have no relationship to ultraviolet radiation, but rather may be
likened to keloid development in the skin.
MANAGEMENT
Because pterygia appear to be linked to environmental exposure, manage asymptomatic or mildly irritative cases
with UV-blocking spectacles and liberal ocular lubrication. Advise patients to avoid smoky or dusty areas as
much as possible. Treat more inflamed or irritated pterygia with topical decongestant/antihistamine
combinations (e.g., Naphcon-A) and/or mild topical corticosteroids (e.g., FML, Vexol) four times daily in the
affected eye.
Surgical excision of pterygia is indicated only for unacceptable cosmesis and/or significant encroachment of the
visual axis. The treatment of choice involves dissection and removal of the fibrous tissue down to the level of
Tenon's capsule. Free conjunctival flaps are then grafted over the bare sclera. Postoperative adjuvant therapy
with b-radiation, topical thiotepa, mitomycin-C and other antimetabolic agents may diminish the chance of
recurrence. In cases that involve significant corneal scarring, lamellar or penetrating keratoplasty may be
indicated.
CLINICAL PEARLS
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A pterygium is a benign clinical entity in most cases. Distinguish between the potentially progressive
pterygium and the less threatening pinguecula-large pingueculae may be difficult to differentiate from
pterygia.
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Conjunctival intraepithelial neoplasia (CIN), a precursor of conjunctival squamous cell carcinoma, is
another clinical entity that must be ruled out in the diagnosis of pterygia. This lesion is generally
unilateral, elevated and gelatinous, with deep irregular vascularization and an ameboid shape. CIN is an
invasive ocular cancer that can inflict significant morbidity. Obtain a biopsy if CIN is suspected.
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Pterygia can affect vision if left unchecked. The corneal degradation may extend beyond the leading
edge of the lesion. This means that the pterygium need not cover the visual axis to inflict significant
visual compromise. Surgery must be performed before vision is affected.
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Follow up on medium- to large-sized pterygia at least once or twice yearly, and include a manifest
refraction, corneal topography, slit lamp evaluation with measurement of the pterygium, and
photodocumentation if possible.
Other reports in this section
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Handbook of Ocular Disease Management - Terrien's Marginal Degeneration
Terrien's Marginal Degeneration
Signs and symptoms: Terrien's marginal degeneration
produces superior nasal peripheral corneal thinning, leaving the
epithelium intact. The condition is often bilateral and may occur at
any age, although it typically occurs in middle-aged males. The
fig01.jpg (5755 bytes)
disease first presents as a peripheral corneal haze. Over time it
exhibits a slowly progressive peripheral corneal thinning with a
sloping central edge that spares the limbus. The eyes are
typically not injected and there is little if any pain, photophobia or
anterior chamber reaction. In fact, aside from increased regular
Terrien's marginal degeneration.
and irregular astigmatism, which may produce visual changes,
(Courtesy Kimberly Reed, O.D.)
patients are often asymptomatic.
Physical signs include an interior circumferential, yellow demarcation line composed of lipid and a fine
pannus, which may resemble a pterygium. The degeneration often progresses in a circumferential
pattern. Perforation is usually only a complication of trauma. Hydrops can occur in severe cases. A
recent report cited a potential association with the chronic, inflammatory skin condition erythema
elevatum diutinum (a rash that appears on the buttocks, wrists, elbows and knees).
Pathophysiology: The etiology of Terrien's marginal degeneration is poorly understood.
Histopathologically, the principle findings include fibrosis, vascularization and phagocytosis of corneal
stromal collagen by histiocytes, with evidence of increased lysosomal activity. A local absence of
Bowman's membrane characterizes the condition; some cases involve breaks in Descemet's
membrane. Autoimmune mechanisms are also potential etiological factors.
Management: Because most patients remain asymptomatic, management of Terrien's marginal
degeneration is largely supportive. Terrien's patients may suffer from periodic episodes of red,
irritated eyes secondary to mild adjacent conjunctival inflammation. These cases often respond
quickly to topical steroidal medications such as prednisolone acetate 0.12% or 1%, or Lotemax
(loteprednol 0.5%) qid.
In cases involving visual symptoms, an astigmatic spectacle correction may be in order. Also, given
the risk of corneal perforation from blunt trauma, prescribing ANSI-standard safety glasses is prudent.
Polycarbonate lenses are mandatory. Contact lenses are a plausible modality for restoring vision;
however, because of complex, irregular astigmatism the fitting is frequently complex as well, calling
for a soft bandage lens with an RGP piggyback. If you attempt a contact lens correction, also
prescribe plano polycarbonate spectacles for safety. When vision is uncorrectable or the risk of
perforation is high, consider surgical options--annular full-thickness penetrating keratoplasty, lamellar
penetrating keratoplasty or large eccentric corneal grafts.
Clinical Pearls:
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Handbook of Ocular Disease Management - Terrien's Marginal Degeneration
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The differential diagnosis of peripheral corneal thinning includes peripheral corneal melt
secondary to collagen vascular diseases such as rheumatoid arthritis and polyarteritis nodosa
(bilateral, typically painful and progressive to perforation); Mooren's ulceration (unilateral or
bilateral, painful corneal thinning with neovascularization); pellucid marginal degeneration
(painless, inferior, peripheral corneal thinning, a variant of keratoconus); furrow degeneration
(painless, peripheral corneal thinning, adjacent to corneal arcus, without vascularization);
dellen (painless, oval thinning secondary to corneal drying); and marginal keratitis secondary
to Staphylococcus hypersensitivity (painful, infiltrate present, inset from limbus).
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Topography can help in diagnosing Terrien's marginal degeneration, which exhibits these
three features: corneal flattening at the juncture of the furrow; corneal steepening 90 degrees
from the flattened area; and a relatively spherical and regular central area.
Other reports in this section
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Handbook of Ocular Disease Management
LIMBAL DERMOID
Signs and Symptoms
Limbal dermoids, also known as epibulbar or
conjunctival dermoids, are generally seen as well-
circumscribed oval mass lesions of the ocular surface.
They arise from the bulbar conjunctiva and virtually
always protrude across the limbus onto the cornea. A
predilection for the inferotemporal limbus has been
noted. Dermoids are firm but "fleshy" in nature, and their
color may range from white to gray to pinkish yellow to
brown, depending upon the specific tissue within the
tumor mass. Often, blood vessels and/or hair follicles
may be seen within or protruding from the dermoid.
Patients are on average quite young, with the majority of
lesions diagnosed before puberty. Dermoids are
Pigmented dermoid.
congenital in nature, but enlarge over time; hence, the
lesion may not be given much regard until the individual reaches adolescence. Smaller lesions are
typically asymptomatic, but larger dermoids may cause discomfort in the form of dry eye symptoms,
conjunctival irritation or lagophthalmos. Visual acuity may also be impacted by larger dermoids, since
these lesions may contribute to the development of astigmatism or encroach onto the visual axis.
Pathophysiology
Dermoids are a form of choristoma--that is, they are benign, congenital tumors composed of tissue
cells atypical to the organ in which they are found. Limbal dermoids consist of thick collagenous
tissue and may also contain elements of skin, fat, gland, muscle, nerve, blood vessels, hair or bone.
Even brain tissue has been found upon histologic analysis of some dermoids.1 The surface generally
consists of simple corneal or conjunctival epithelium.
Dermoids may represent an isolated finding, or may be seen in conjunction with other ocular or
oculosystemic disorders, including eyelid and iris colobomas, microphthalmos, and retinal or choroidal
defects. Fully 30% of dermoids are associated with systemic abnormalities, including craniofacial
abnormalities (e.g., Goldenhar syndrome), nevus flammeus and neurofibromatosis. However, most
limbal dermoids represent sporadic occurrences, and are not caused by known exposure to toxins or
mechanical irritants.
Management
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The preferred management of a limbal dermoid depends upon the extent of the lesion and the
disposition of the patient. Small, asymptomatic lesions can simply be left alone, since there is no
likelihood of malignant transformation. Mild irritation can be managed with ocular lubricants or even a
short course of topical corticosteroids (e.g., prednisolone sodium phosphate 1%, Lotemax, or Alrex
[Bausch & Lomb], q2h-qid x 3-7 days). Epilation of exposed hair follicles may also help palliate the
patient. When definitive treatment is indicated--as in the case of profound cosmetic concern, physical
irritation or visual impairment--surgical excision is the preferred technique. Surgery must be
performed with caution however, since these lesions are occasionally contiguous with tissue of the
sclera and orbit.
Generally, the surgical procedure of choice is superficial sclerokeratectomy with excisional biopsy.
When deeper excisions need to be performed, lamellar keratoplasty has been shown to be safe and
effective.2-4 Preopera-tive evaluation with ultrasound biomicroscopy may well improve the
visualization of the lesion, hence enhancing surgical planning and the potential outcome.5,6
Clinical Pearls
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Limbal dermoids show no specific predilections with regard to sex or race. The appearance
may vary depending upon the patient's skin pigmentation; melanosis oculi can influence
dermoid coloration.
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The most notable systemic condition associated with limbal dermoids is Goldenhar syndrome,
a craniofacial disorder that also presents with characteristic preauricular skin tags and
associated hearing loss. In addition, these patients may show underdeveloped facial muscles,
malformation of the mouth or ears, spinal or cervical vertebrae problems, cleft lip/ palate, renal
or cardiac disorders, and learning disabilities. Families of pediatric patients with limbal
dermoids should be alerted to the possibility of Goldenhar syndrome, and referred for
appropriate testing.
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Young patients with limbal dermoids that encroach the visual axis are at risk for developing
deprivation or meridional amblyopia. Specific testing, including potential acuity measurement
or interferometry, should be performed on those youngsters with dermoids and reduced visual
acuity. The finding of associated amblyopia is an absolute indication for excision of the lesion,
followed by a subsequent course of vision therapy.
1. Emamy H, Ahmadian H. Limbal dermoid with ectopic brain tissue. Report of a case and review of the
literature. Arch Ophthalmol 1977; 95(12):2201-2.
2. Mader TH, Stulting D. Technique for the removal of limbal dermoids. Cornea 1998; 17(1):66-7.
3. Scott JA, Tan DT. Therapeutic lamellar kerat oplasty for limbal dermoids. Ophthalmology 2001; 108
(10):1858-67.
4. Panda A, Ghose S, Khokhar S, et al. Surgical outcomes of epibulbar dermoids. J Pediatr Ophthalmol
Strabismus 2002; 39(1):20-5.
5. Hoops JP, Ludwig K, Boergen KP, et al. Preoperative evaluation of limbal dermoids using high-resolution
biomicroscopy. Graefes Arch Clin Exp Ophthalmol 2001; 239(6):459-61.
6. Grant CA, Azar D. Ultrasound biomicroscopy in the diagnosis and management of limbal dermoid. Am J
Ophthalmol 1999; 128(3):365-7.
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Handbook of Ocular Disease Management
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Handbook of Ocular Disease Management - ACUTE ANGLE CLOSURE GLAUCOMA
ACUTE ANGLE CLOSURE GLAUCOMA
SIGNS AND SYMPTOMS
Patients with angle closure glaucoma manifest symptoms of ocular and facial pain, unilateral blurring of vision,
photopsiae in the form of colored haloes around lights, and occasionally nausea and vomiting. Acuity may be
reduced significantly in the involved eye, often to 20/80 or worse.
The hallmark signs of angle closure include significantly elevated intraocular pressure, a closed angle upon
gonioscopic evaluation, deep conjunctival and episcleral injection in a circumlimbal fashion, and a fixed, mid-
dilated pupil. Upon slit-lamp examination, you may also see an edematous or "steamy" cornea and shallow
anterior chamber.
Applanation tonometry may reveal IOP in the range of 30 to 60mm Hg, or even higher in some cases.
Gonioscopy, which may prove difficult because of microcystic corneal edema, reveals no visible angle
structures without indentation. There may be evidence of previous angle closure episodes in the form of
peripheral anterior synechiae (PAS) in the fellow eye.
PATHOPHYSIOLOGY
Angle closure occurs when the peripheral iris physically opposes the trabecular meshwork or corneal
endothelium and impedes aqueous outflow. Several mechanisms are possible. The most common etiology of
angle closure is pupillary block, whereby the flow of aqueous from the posterior to anterior chamber is inhibited,
causing iris bombé. This may be simply due to genetic predisposition and anterior segment anatomy (primary
pupil block), or from posterior synechiae, lenticular enlargement or displacement of the lens or IOL (secondary
pupil block).
Another mechanism which may induce angle closure involves an abnormal configuration of the iris, the so-
called "plateau iris syndrome." Patients with this presentation may boast a deep anterior chamber centrally;
however, the iris demonstrates an unusual laxity, coming into close approximation with the angle peripherally.
These patients may be prone to "angle crowding" and subsequent closure during physiologic or pharmacologic
dilation. Other etiologies of angle closure without pupil block include neovascular membranes inducing PAS,
anterior uveal displacement (such as in choroidal detachment) or, rarely, posterior segment inflammation or
tumors.
MANAGEMENT
The paramount concern in managing an angle closure attack is to lower IOP quickly. Your choice of primary
medication depends upon the pressure at presentation. As most miotics are ineffective at pressures over 40mm
Hg due to iris ischemia, immediately treat such patients with a beta-blocker of 0.5% concentration and/or
apraclonidine 1%.
Next, perform corneal compression with a gonioprism to aid in lowering the IOP by forcing aqueous into the
trabeculum and temporarily opening the angle. It may be necessary to use topical glycerin to clear the cornea if
there is significant edema. Perform tonometry every 15 minutes after initiating therapy.
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Handbook of Ocular Disease Management - ACUTE ANGLE CLOSURE GLAUCOMA
If the patient does not achieve significant reduction in IOP after 45 minutes, administer an oral carbonic
anhydrase inhibitor (acetazolamide 2 x 250mg tablets). You may also wish to use a hyperosmotic agent such as
three to five ounces of oral glycerin or isosorbide over ice. Once the IOP is below 40mm Hg, instill pilocarpine
2% as well as prednisolone acetate 1% every 15 minutes to abate the attack and reopen the angle. It is safe to
discontinue this regimen when the IOP is below 30mm Hg and the angle structures are again visible with
gonioscopy. Maintain the patient on the following medications: pilocarpine 2% QID, prednisolone acetate 1%
QID, timolol (or equivalent) 0.5% BID, and oral acetazolamide 500mg BID.
When the inflammation has diminished and the AC is quiet, refer the patient for a peripheral iridotomy. This
provides a secondary outflow channel for aqueous, and commonly causes a permanent anatomical "deepening"
of the anterior chamber.
CLINICAL PEARLS
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The most important consideration in handling an acute angle closure attack is accurate diagnosis and
prompt intervention. First distinguish between angle closure glaucoma and other acute open angle
conditions such as uveitic glaucoma, glaucomatocyclitic crisis and phacolytic glaucoma. Once you have
established angle closure as the cause, you must also differentiate the nature of the attack, whether due to
primary pupillary block, plateau iris, or secondary pupillary block. If you are uncertain of the etiology or
if an inflammatory glaucoma is present, do not use a miotic, as this will only exacerbate the condition.
Other Reports in This Section
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Handbook of Ocular Disease Management - Angle Recession Glaucoma
ANGLE RECESSION GLAUCOMA
SIGNS AND SYMPTOMS
Angle recession glaucoma may affect patients of any age. The patient
remains asymptomatic, and will report a history of blunt trauma to the
involved eye, often years earlier. There may be an associated traumatic
cataract.
Expect a rise in IOP, which may be substantial. An unexplained IOP rise in the fellow eye often occurs in
unilateral cases. There may be an associated iridodyalysis in severe cases. Gonioscopy will reveal a deepening
of the angle recess and the appearance of excessive gray tissue (ciliary body) posterior to the scleral spur.
PATHOPHYSIOLOGY
In angle recession, blunt trauma to the eye tears the ciliary body between the longitudinal and meridional
muscles. Frequently, there is hyphema at the time of trauma.
Intraocular pressure does not rise until long after the initial injury. Approximately 20 percent of patients with
angle recession develop secondary glaucoma, depending on the extent of angle recession. Typically, two-thirds
of the angle must be compromised in order for glaucoma to develop.
Controversy surrounds the etiology of IOP rise in traumatic angle recession. One theory involves direct
traumatic damage to the trabecular meshwork. Another theory contends that particulate matter such as pigment
and hemosiderin released at the initial trauma damages the trabecular meshwork, causing scarring and poor
filtration. Yet another thought suggests that endothelial cells migrate and proliferate over the trabecular
meshwork in response to trauma, forming a Descemet's-like membrane that blocks filtration. Interestingly,
there seems to be a higher than expected incidence of POAG in the non-traumatized fellow eye, leading some
to speculate that these angle recession eyes have a predisposition to IOP elevation.
MANAGEMENT
Miotics, prostaglandin analogs and argon laser trabeculoplasty are rather ineffective in managing angle
recession glaucoma since the outflow structures have likely been compromised. More appropriate topical
medications include aqueous suppressants such as beta blockers, carbonic anhydrase inhibitors and alpha
adrenergic agonists. If medical therapy fails to control IOP, filtering surgery remains an excellent option.
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Handbook of Ocular Disease Management - Angle Recession Glaucoma
CLINICAL PEARLS
●
In cases of unilateral glaucoma, look for a history of trauma.
●
In many cases of angle recession glaucoma, the angle appears relatively normal, except that it shows
more of the posterior angle structures than typical. By examining only the suspect eye, you may
misread the diagnosis. In unilateral cases, compare the suspect eye with the normal fellow eye to reveal
asymmetry between the angles.
Other Reports in This Section
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Angle Recession Glaucoma
●
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Handbook of Ocular Disease Management - Anterior Uveitis
Anterior Uveitis
Signs and Symptoms: The typical presentation of anterior
uveitis involves pain, photophobia and hyperlacrimation. Patients
report a deep, dull aching of the involved eye and surrounding
orbit. Associated sensitivity to lights may be severe. Excessive
tearing results secondary to increased neural stimulation of the
lacrimal gland, and is not associated with a foreign-body
sensation.
Visual acuity is variable, ranging from mild blur to significant
vision loss if synechia or a cyclitic membrane are present.
Circumlimbal flush in anterior
External exam may reveal mild to moderate lid swelling, resulting
uveitis.
in pseudoptosis. A deep, perilimbal injection of the conjunctiva
and episclera is typical, while the palpebral conjunctiva is characteristically normal. The cornea may
display mild edema upon biomicroscopy.
The hallmark signs of anterior uveitis are cells and flare in the anterior chamber. If the anterior
chamber reaction is significant, small gray to brown endothelial deposits known as keratic precipitates
may arise. This can then lead to endothelial cell dysfunction and the corneal edema.
Iris findings may include adhesions to the lens capsule (posterior synechia) or, less commonly, to the
peripheral cornea (anterior synechia). Additionally, granulomatous nodules may appear on the
surface of the iris stroma. Intraocular pressure is initially reduced in the involved eye, due to secretory
hypotony of the ciliary body. However, as the reaction persists, inflammatory by-products may
accumulate in the trabeculum. If this debris builds significantly, and if the ciliary body resumes its
normal secretory output, the pressure may rise sharply, resulting in a secondary uveitic glaucoma.
Pathophysiology: Uveitis, as the name implies, represents an inflammation of the uveal tissues,
chiefly the iris and ciliary body. This inflammation may be associated with underlying systemic
disease or autoimmunity, or it may occur as a direct result of ocular trauma. Occasionally,
inflammatory reactions in adjacent tissues--for example, keratitis--can induce a secondary uveitis.
Both acute and chronic forms of anterior uveitis are clinically recognizable. The chronic form is more
often associated with a host of systemic disorders (see table). Chronic uveitis most likely occurs due
to an immunopathological mechanism that is not fully understood.
Management: Your two primary goals in the manage ment of anterior uveitis should be to first
immobilize the iris to decrease the pain and prevent synechia, and to aggressively quell the
inflammatory response.
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Cycloplegia is in order. Use either scopolamine 0.25% bid-qid, or
atropine 1% bid, depending upon the severity of the reaction.
Prescribe topical steroids, such as prednisolone acetate 1%, at
least q1-2h initially, even more frequently if warranted. We
commonly employ a loading dose of one drop every 15 minutes
for six hours, then taper to q1-2h. If posterior synechia is present,
attempt to break the adhesions in the office using 1% atropine in
conjunction with 10% phenylephrine. Address significant
secondary elevations in IOP (>26mm Hg) with standard aqueous
Keratic precipitates in anterior
suppressant agents. Avoid pilocarpine in uveitic glaucoma
uveitis.
because it will only worsen the inflammatory response by
mobilizing the uveal tissues. Likewise, avoid prostglandin-like
medications. After you initiate treatment, re-evaluate patients every 1-7 days, depending on the
severity of the reaction. As the condition resolves, you may discontinue the cycloplegics and taper the
topical steroids to qid or tid. Generally, it is better to taper slowly rather than abruptly; patients may
need to remain on steroid drops daily or every other day for several weeks to months. In recalcitrant
cases of uveitis that do not respond to conventional therapy, injectable depot steroids (e.g.,
methylprednisolone 60mg), oral corticosteroids (prednisone 60-80mg), or other immunosupressant
medications are indicated.
Clinical Pearls:
●
Acute anterior uveitis that we see in
Systemic Disorders Associated
optometric practice results most
With Chronic Uveitis
commonly from blunt ocular trauma. In
• Ankylosing spondylitis.
most instances, these cases resolve
without incident and do not recur when
• Behçet's syndrome.
properly managed.
• Inflammatory bowel disease.
●
Consider recurrent uveitis--defined as
• Juvenile rheumatoid arthritis.
three or more unexplained incidents--
• Reiter's syndrome.
secondary to underlying systemic
• Sarcoidosis.
inflammatory disease until proven
• Syphilis.
otherwise.
• Tuberculosis.
●
Hematological testing is indicated for any
• Lyme disease.
recurrent, chronic, or bilateral
presentation. A standard battery of
laboratory tests should include: complete blood count (CBC) with differential; antinuclear
antibody (ANA); HLA-B27; rheumatoid factor (RF); angiotensin-converting enzyme (ACE);
purified protein derivative (PPD); fluorescent treponemal antibody absorption (FTA-ABS); and
rapid plasma reagin (RPR). A chest X-ray is important for identifying sarcoidosis and
tuberculosis.
●
Treat aggressively and follow closely. The goal of therapy is to have no cells with the patient
on little or no steroids, and to have no therapy-related complications.
●
One additional point: Always perform a comprehensive, dilated fundus evaluation in these
cases. Anterior uveitis may actually constitute a "spillover" of posterior ocular inflammation.
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Other reports in this section
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Handbook of Ocular Disease Management - Ciliary-Block Glaucoma
Ciliary-Block Glaucoma
Signs and Symptoms: Patients with ciliary-block glaucoma are typically hyperopic with small or
nanophthalmic eyes. The condition usually develops after ocular surgery--typically glaucoma surgery,
and most commonly filtration surgery, but also peripheral iridectomy or cataract extraction. There may
have been a period of hypotony due to over-filtration following glaucoma surgery. At the slit lamp,
there will be a shallow or non-existent anterior chamber. Also, they may have a history of beginning
miotic therapy. Patients who develop significant inflammation, such as scleritis, may also develop
ciliary-block glaucoma.
Patients with ciliary-block glaucoma will present with intense pain, ocular injection, a cloudy cornea
with copious edema and subsequent blurred vision, a flat anterior chamber and elevated intraocular
pressure. The flat anterior chamber frequently appears even with patent iridotomies or iridectomies.
Pathophysiology: Classic ciliary-block glaucoma occurs following filtering surgery, typically in an
eye with a preexisting narrow angle and shallow chamber. Eyes with shallow anterior chambers
undergoing surgery are at risk for the condition. One theory holds that these patients have very small
uveal effusions due to ocular hypotony from over-filtration after surgery. These small effusions
produce a rotation of the ciliary body with subsequent complete angle closure. Thus, according to this
theory, ciliary block does not actually occur. In some cases, a retro-iris tumor can physically push the
iris and lens into apposition and mimic ciliary-block glaucoma. In rare patients who are anatomically
predisposed, the use of pilocarpine can precipitate ciliary-block glaucoma.
The more widely accepted theory holds that a tight apposition of ciliary processes to the lens or
anterior vitreous forms either after surgery or due to a natural predisposition. This prevents the
aqueous from flowing into the anterior chamber, and instead diverts it into the vitreous cavity. An
abnormally impermeable anterior hyaloid face may play a role, in that the aqueous cannot diffuse
from the vitreous and thus expands the volume of vitreous. This pushes the lens and iris towards the
cornea with subsequent shallowing of the anterior chamber and closure of the angles.
The classic appearance is a shallow axial depth (lens-corneal distance) and a shallow peripheral
depth (iris-corneal distance). In ciliary-block glaucoma, iridotomy will have no effect; the hallmark of
ciliary-block glaucoma is a closed angle and shallow chamber with patent iridotomy or iridectomy.
Management: The goal of management of ciliary-block glaucoma first aims medically to break the
apposition of the ciliary body and ciliary processes to the lens and anterior vitreous, relax the ciliary
body and lens zonules, and allow the lens to relax posteriorly. Atropine 1% and phenylephrine 2.5%
or 10% (both bid) can accomplish this. Aqueous suppressants will temporize the intraocular pressure
and topical steroids will ameliorate the inflammation. Miotics are strictly contraindicated; they can
precipitate this condition. You can use oral hyperosmotic agents to shrink the vitreous. Medical
therapy is used initially in an attempt to manage ciliary block glaucoma.
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Handbook of Ocular Disease Management - Ciliary-Block Glaucoma
If medical management does not succeed, there are surgical options. The first involves disruption of
the anterior hyaloid face to allow aqueous to escape from the vitreous cavity. This potentially redirects
the aqueous into the anterior rather than the posterior chamber. The most common method involves
Nd:YAG laser photodisruption of the anterior vitreous face through an iridectomy or iridotomy hole or
through the pupil. This may create an opening for aqueous to reach the anterior chamber.
Vitrectomy is a more invasive option. Here, the surgeon "debulks" the vitreous, relaxing the iris and
deepening the anterior chamber. The procedure also removes pockets of aqueous within the vitreous
and disrupts the anterior vitreous face; this may rectify the blockage that prevented the misdirected
aqueous from ultimately getting through the pupil.
Unfortunately, after successful treatment of the ciliary-block glaucoma, the angle may remain closed
due to extensive peripheral anterior synechiae. If more than half of the angle remains closed,
intraocular pressure will remain permanently elevated despite successful treatment. In this case, the
surgeon may try to break the peripheral anterior synechiae with a gonio-synechialysis. In an inflamed
eye, filtration is likely to fail, even with the use of antimetabolites. For this reason, the surgeon will
typically use a tube shunt. If synechiae closes the angle, a tube shunt is mandatory.
Clinical Pearls:
●
Pupillary block is the most common condition that mimics ciliary-block glaucoma. Laser
iridotomy will relieve papillary-block angle closure, but will have no effect on ciliary-block
glaucoma. Laser iridotomy is necessary to differentiate these two conditions.
●
Choroidal effusion with a shallow chamber, particularly after glaucoma filtration surgery, is the
second most common differential diagnosis for ciliary- block glaucoma. Ophthalmoscopy will
show large effusions. Small, suprachoroidal effusions can cause an anterior rotation of the
ciliary body and precipitate this condition. However, these small effusions are typically only
detectable with ultrasound biomicroscopy.
Other reports in this section
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Ciliary-Block Glaucoma
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Handbook of Ocular Disease Management - Crystalline Lens Subluxation
Crystalline Lens Subluxation
Signs and Symptoms: While crystalline lens subluxation can
occur in any patient, these three profiles are most prone:
significant blunt trauma to the eye or head; systemic conditions
such as Marfan's syndrome, homocystinuria, hyperlysinuria,
fig01.jpg (5755 bytes)
familial ectopia lentis, sulfite oxidase deficiency, Weill-
Marchesani syndrome, aniridia and Ehlers-Danlos syndrome;
hypermature cataract in which zonular support has been lost.
Symptoms of lens subluxation includes visual disturbance from
Crystalline lens subluxation as seen
extreme hyperopic or myopic shift, astigmatism or acquired
without (above) and with (below)
aphakia. Occasionally, the vision fluctuates dramatically as the
retroillumination.
patient may alternate between phakic and aphakic vision.
Monocular diplopia may also manifest. In most cases, there are
no physical sensations except when the lens blocks the pupil,
leading to secondary angle closure. In that case, the patient will
manifest all of the symptoms of an acute angle closure glaucoma
attack.
At the slit lamp you will note a displaced crystalline lens. This
appears as a black crescent at the edge of the lens against a red
reflex from the fundus. The lens can be up and out, down and in,
down and out, nasal or temporal, or completely displaced into the
posterior or anterior chamber. Phacodonesis (tremulousness of the lens due to loss of zonular
support) and iridodonesis (tremulousness of the iris) may also exist. With pupillary block, there may
be inflammation, corneal edema, angle closure and markedly elevated intraocular pressure.
Pathophysiology: Subluxation implies displacement of the crystalline lens, whereas luxation refers
to a lens that is totally dislocated. The term ectopia lentis has been used interchangeably with
subluxation, although this term should be reserved for bilateral cases.
Lens subluxation can be either acquired or due to congenital systemic causes. Infants are rarely born
with displaced lenses; rather, they develop due to a predisposing systemic condition.
Acquired subluxation is slightly more common than lens displacement associated with underlying
systemic disorders. Trauma accounts for a large percentage of all acquired lens subluxations, with
mechanical stretching of the zonules. This occurs as the eye is compressed in an anterior-posterior
direction, such as with impact by a fist or ball. The subsequent distention of the globe in the medial-
lateral plane ruptures the zonular fibers. Other acquired causes include chronic cyclitis, syphilis,
buphthalmos, ciliary body tumor and severe or pathological myopia.
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The pathophysiologic mechanism of lens subluxation from congenital causes varies depending on the
condition. The direction of displacement in each case is characteristic, although not completely
diagnostic. In Marfan's syndrome, the lenses tend to displace supero-temporally due to abnormal
collagen vascular tissue and faulty lens zonules. It is typically present at birth and is non-progressive.
Because the zonules are still attached to the lens, some accommodation remains.
Homocystinuria, a defect in amino acid metabolism, results in brittle zonules that rupture. This allows
the lens to displace inferonasally or even into the anterior chamber. There is no accommodation, and
the condition may progress.
Two other conditions worth mentioning are simple ectopia lentis and ectopia lentis et pupillae. Simple
ectopia lentis is an autosomal-dominant condition where the lenses are dislocated superotemporally,
but there are no other associated systemic abnormalities. Ectopia lentis et pupillae is likewise an
isolated inherited condition, albeit autosomal-recessive, where the lenses displace temporally in
opposite directions.
The main concern with lens subluxation is the development of secondary angle closure glaucoma.
Anytime the crystalline lens displaces, there is always the possibility that the lens can come into
apposition with the back surface of the iris (or the front surface of the iris during complete lens
dislocation into the anterior chamber). This will lead to pupillary block, iris bombé and secondary
angle closure. Also, if the lens completely dislocates into the anterior chamber, the lens may touch
the cornea, irreversibly damaging the endothelial cells with subsequent corneal edema and
decompensation.
Management: Extraction of a dislocated lens can be difficult, so a subluxated lens itself is not
sufficient reason to pursue surgery. In the absence of pupillary-block glaucoma, corneal
decompensation, inflammation or intractable visual disability, leave the subluxated lens alone in favor
of non-surgical options. For stable induced refractive errors, visual correction with glasses or contact
lenses may be an option.
If the lens luxates into the posterior chamber but no inflammation ensues, simply monitor the
condition. However, if inflammation does occur and the threat of retinal damage presents, vitrectomy
and lens extraction are necessary.
Avoid dilating cases in which you suspect loss of zonular adherence (as with hypermature cataracts)
with subsequent risk of dislocation into the anterior chamber until you obtain a surgical consultation. If
the lens has already spontaneously dislocated into the anterior chamber, or where the patient was
dilated with subsequent anterior dislocation, follow this protocol: Recline the patient (who can be
dilated, if the dislocation happened spontaneously), then carefully manipulate the head until the lens
falls back into place in the fossa. Apply pilocarpine solution and obtain a surgical consultation.
If pupillary-block, angle-closure glaucoma develops, laser peripheral iridotomy is indicated as soon as
possible. However, this rarely manages the condition successfully. Thus, the patient should then
undergo lens extraction with intraocular lens implantation. While some surgeons have had success
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Handbook of Ocular Disease Management - Crystalline Lens Subluxation
with posterior chamber implants, anterior chamber lenses are typically the modality of choice.
Clinical Pearls:
●
In any case of lens dislocation, a strong possibility of pupillary block and secondary angle
closure glaucoma exists.
●
Eighty percent of patients with Marfan's syndrome develop lens subluxation.1
●
The mere fact that a lens is subluxed is not sufficient reason to surgically extract the lens.
●
Symptomatic subluxation can be managed effectively with opaque contact lenses or long-term
pilocarpine therapy.
1. Cross HE, Jensen AD. Ocular manifestations in the Marfan's syndrome and homocystenuria. Am J
Ophthalmol 1973; 75:405.
Other reports in this section
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Crystalline Lens Subluxation
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●
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Handbook of Ocular Disease Management - Hyphema
HYPHEMA
SIGNS AND SYMPTOMS
Patients may present with blurred vision, pain, photophobia and
tearing following blunt, concussive injury to the eye or orbit.
Hyphemas (blood in the anterior chamber) are described by the
amount of anterior chamber (AC) they occupy:
Grade 1 = less than one-quarter of the visible volume of the AC
Grade 2 = one-quarter to one-half of the visible volume of the AC
Grade 3 = one-half to three-quarters of the visible volume of the AC
Grade 4 = complete filling of the visible AC
The term "eight-ball hemorrhage" is reserved for completely filled anterior chambers with black-colored clots.
PATHOPHYSIOLOGY
There are two suggested mechanisms of hyphema formation. Either direct, contusive forces cause mechanical
tearing of the fragile blood vasculature of the iris and/or angle, or concussive trauma creates rapidly rising
intravascular pressure within these vessels, resulting in rupture.
Blood in the AC is not by itself necessarily harmful. However if quantities are sufficient it may obstruct the
outflow of aqueous humor, resulting in glaucoma. Hemolytic glaucoma results from direct obstruction of the
trabecular meshwork by fresh blood. Hemosiderosic glaucoma results from trabecular meshwork obstruction
from degrading hemoglobin. Ghost cell glaucoma results from trabecular meshwork obstruction by the
skeletons of the disintegrating red blood cells. Finally, any external force strong enough to produce internal
bleeding is also sufficiently strong to produce direct damage to the adjacent trabecular meshwork, resulting in
sluggish aqueous drainage (late glaucoma).
MANAGEMENT
A thorough history is critical. Circumstances surrounding the event, current medicines and previous ocular
history are important pieces of data. Bleeding in the eye warrants questioning concerning systemic blood
disorders such as sickle cell anemia, hemophilia and Von Willebrand's disease (vascular hemophilia). If the
patient is a poor historian or questions arise regarding systemic health, order systemic tests for sickle cell
anemia (sickle prep or sickle dex) and bleeding disorders (PT and PTT).
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Handbook of Ocular Disease Management - Hyphema
Ocular examination should include an evaluation of the adnexa (X-ray, CT scan to rule out fracture or
entrapment) cornea (to rule out perforation), sclera (to rule out ruptured globe), anterior chamber, lens, vitreous
and retina. If a clear view of the fundus is obstructed by the hyphema or vitreous hemorrhage, perform or refer
for a B-scan ultrasound of the globe.
Whether these individuals should be hospitalized is controversial. Most practitioners manage uncomplicated
hyphemas (grade 1) without hospital admission. Cycloplege the patient with atropine 1% BID/QID and
prescribe a steroid such as Pred Forte or Vexol Q2H/QID. If intraocular pressure is above 27mm Hg, it should
be controlled using topical beta-blockers BID. When IOP requires acute attention (i.e., over 35mm Hg)
prescribe acetazolamide 500mg PO BID, barring systemic contraindications, until the pressure is adequately
controlled. If there are corneal epithelial defects, Rx a topical antibiotic prophylactically. Instruct the patient to
limit activity to the bathroom and bed rest, laying with the head elevated at an angle of 30 degrees. Provide an
eye shield for additional protection.
To prevent re-bleeding, use only acetaminophen to manage pain; avoid aspirin and ibuprofen. Referral for
surgical evaluation is indicated if there is corneal blood staining, if IOP is greater than 60mm Hg, if there is an
eight-ball hemorrhage or if the IOP remains above 35 for seven days. Follow up with VA, slit lamp, IOP and
dilated fundus exam for four consecutive days, then as necessary.
CLINICAL PEARLS
●
Gonioscopy is contraindicated because it increases the risk of re-bleeding. However, up to 50 percent of
patients with hyphema possess angle recession and the possibility of developing a secondary traumatic
late glaucoma. Monitor the IOP of these patients regularly. The onset of secondary glaucoma is between
12 months and 50 years. Perform gonioscopy after the event has resolved and the risk of re-bleeding has
passed.
●
Aminocaproic acid (Amicar 50mg/kg), an antifibrinolytic, has been advocated by some to reduce the
risk of re-bleeding. One of its potential side effects is severe nausea and vomiting, a contraindication in
patients with hyphema. The medicine seems to function best in children but is not universally accepted
and remains controversial.
Other Reports in This Section
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Hyphema
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Handbook of Ocular Disease Management - Lens Induced Glaucomas
LENS INDUCED GLAUCOMAS
SIGNS AND SYMPTOMS
The lens induced glaucoma patient is typically elderly, with a
history of cataracts. There are four types of glaucomas associated
with lens complications (excluding cases of lens displacement in
ectopia lentis):
●
phacolytic glaucoma
●
lens particle glaucoma
●
phacoanaphylactic uveitis
●
phacomorphic glaucoma
In all of these cases, the glaucoma is typically very symptomatic with pain and redness in the involved eye, and
cells and flare in the anterior chamber. Frequently, an advanced cataract in the involved eye severely reduces
vision.
PATHOPHYSIOLOGY
Phacolytic glaucoma This condition involves a hypermature cataract with severe visual reduction (typically
light perception). It's characterized by acute onset of pain and redness and IOPs often of 35mm Hg or greater.
There is liquefaction of the lens nucleus and cortex, and attenuation of the capsule with the release of lens
proteins into the anterior chamber. Macrophages engulf the lens proteins, become bloated, and block trabecular
outflow. The angle remains open, though in some cases peripheral anterior synechiae may develop.
Lens particle glaucoma The mechanism of lens particle glaucoma resembles that of phacolytic glaucoma,
except that there is a history of surgery or trauma that releases the lens proteins into the anterior chamber and
initiates a macrophage-driven inflammatory reaction. The angle remains open.
Phacoanaphylactic uveitis This is a chronic uveitis that occurs one to 14 days following cataract extraction or
lens trauma. This mechanism is similar to the previous two types of glaucoma, except that inflammatory cells
are not limited to macrophages. Also, there is considerable flare and mutton-fat keratic precipitates, and a
propensity for synechiae formation. The angle may be open or closed.
Phacomorphic glaucoma In this case, an increase of lens thickness from an advancing cataract leads to a
relative pupil block, posterior bombé and angle closure. The intumescence often develops quickly. Typically,
the cataract reduces vision severely. The angle in this glaucoma is closed.
MANAGEMENT
Employ topical beta blockers, carbonic anhydrase inhibitors and alpha adrenergic agonists to temporize the
IOP. Avoid miotics and prostaglandin analogs in cases where inflammation is present. In cases where there is
significant anterior segment inflammation, use topical steroids to quell the inflammation. In cases where the
lens precipitates a secondary glaucoma, the best management is surgical lens removal.
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CLINICAL PEARLS
●
In cases of severe granulomatous uveitis with IOP rise following cataract extraction, consider
phacoanaphylactic uveitis.
●
In patients with hypermature cataracts and shallow anterior chambers with angle closure, consider
phacomorphic glaucoma, especially if the fellow lens has less intumescence and there is a deeper
chamber.
●
Phacomorphic and phacolytic glaucoma develop only in eyes with hypermature cataracts. Vision
typically ranges from 20/400 to light perception. If vision is better than 20/400, consider another cause
for the glaucoma.
●
In cases where there is phacomorphic glaucoma in a nanophthalmic eye, surgical excision of the
cataract is associated with severe complications of choroidal detachment and hemorrhage. In these
cases, you may prefer medical therapy and laser iridotomy rather than surgical management.
Other Reports in This Section
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●
●
●
●
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●
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Lens Induced Glaucoma
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Handbook of Ocular Disease Management - New Insights Into Treating Ocular Hypertension
New Insights Into Treating Ocular Hypertension
In the past, when a patient's intraocular pressure (IOP) was elevated with normal visual fields and
optic nerves, you faced a dilemma. On one hand, you could initiate IOP reduction therapy, knowing
full well that the patient might never develop a problem from the elevated IOP, and would be incurring
the expense and risks associated with therapy. On the other hand, you could watch for glaucomatous
change before initiating therapy, knowing that 20% to 50% of the optic nerve fibers may be lost before
you could make a conclusive diagnosis. Perhaps the visual field defect that developed would be a
troublesome paracentral scotoma, or the initial damage might make the remaining fibers more
susceptible to further damage.
This year we saw the publication of The Ocular Hypertension Treatment Study (OHTS) results and its
companion piece. This study has greatly increased our understanding of ocular hypertension and the
risk for developing glaucoma.
Notably, the study concluded that lowering IOP in patients with ocular hypertension reduced the risk
of developing glaucoma in five years from 9.5% to 4.4%.1 Thus, IOP reduction in ocular hypertension
did benefit some patients. However, it is also easy to see that initiating therapy on every patient with
ocular hypertension would result in gross over-treatment.
OHTS also attempted to identify which patients would most likely benefit from treatment.2 There were
some surprising results. While race (blacks) and family history were expected to be predictive of the
development of POAG, they weren't strongly predictive. Surprisingly, the presence of diabetes
seemed to protect patients from the development of glaucoma. Not unexpectedly, older age, larger
initial cup-to-disc ratio, and higher IOP were predictive of glaucoma.
However, the factor that was most predictive was the presence of a thin central cornea. Patients with
a central corneal thickness of 555µm or less had a three-fold greater risk of developing POAG than
those with a central corneal thickness of 588µm or greater.
The theory holds that the rigidity of a thick cornea artificially elevates the Goldmann applanation
measurement of IOP and a thin cornea consequently lowers the reading of the true IOP, though other
unknown factors may contribute to this finding.
Central corneal thickness appears to be a powerful predictor of the progression from ocular
hypertension to POAG. The study shows patients with thin central corneas are likely to benefit most
from IOP reduction. Rarely are the conclusions of a landmark study so emphatic: At this time,
measurement of central corneal thickness is necessary to accurately manage patients with ocular
hypertension.
1. Kass MA, Heurer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study. A randomized
trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open
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Handbook of Ocular Disease Management - New Insights Into Treating Ocular Hypertension
angle glaucoma. Arch Ophthalmol 2002;120:701-13.
2. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that
predict the onset of primary open angle glaucoma. Arch Ophthalmol 2002; 120:714-20
Other reports in this section
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New Insights Into Treating Ocular Hypertension
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Handbook of Ocular Disease Management - Pigment Dispersion Syndrome and Pigmentary Glaucoma
Pigment Dispersion Syndrome and Pigmentary Glaucoma
Signs and Symptoms: Pigment dispersion syndrome (PDS) is
generally an asymptomatic disorder discovered during routine
ophthalmic evaluation. Pigmentary glaucoma (PG), a sequelae of
PDS, may likewise be asymptomatic; or patients may complain
of symptoms related to episodic IOP rises, such as colored
fig01.jpg (5755 bytes)
haloes around lights, blurred vision or subtle ocular pain,
particularly after exercise. Both conditions occur most often in
young, white males between ages 20 to 40.
At the slit lamp, patients with PDS and PG demonstrate bilateral
Transillumination defects of the iris
in pigment dispersion syndrome
liberation of iris pigment within the anterior chamber. Often, this
and pigmentary glaucoma.
appears as a granular brown vertical band along the corneal
endothelium (Krukenberg's spindle). Pigment dusting may be
evident on the lens, the iris surface and Schwalbe's line.
Gonioscopy may reveal dense pigmentation resembling melted
chocolate covering the trabecular meshwork for 360 degrees,
most prominently in the inferior quadrant. The angle itself
remains patent, and in some cases appears atypically wide
open. Radial, spoke-like transillumination defects of the mid-
peripheral iris are another common finding.
Heavy pigmentation of the
trabecular meshwork in pigment
While IOP does not alter in PDS, it may rise sharply in cases of
dispersion syndrome and
pigmentary glaucoma, particularly after vigorous exercise or
pigmentary glaucoma.
pharmacological dilation. Likewise, patients with PDS present a
normal optic nerve, while those with PG manifest glaucomatous optic atrophy and field loss.
Blacks--mostly middle-age to elderly females--tend to get a distinctly different form of pigmentary
glaucoma. These patients typically present with no iris transillumination defects, and minimal
endothelial pigment accumulation which is sometimes clinically undetectable. The amount of
endothelial pigment accumulation does not predict the amount of pigment collected in the trabecular
meshwork. Frequently, the patient will demonstrate pigment accumulation at the anterior lens
equator.
Pathophysiology: Pigment dispersion results from the proximity between the posterior iris pigment
epithelium and the zonular fibers of the lens. The abrasive physical contact leads to mechanical
disruption of the iris surface and release of pigment granules into the posterior chamber, which
follows the flow of aqueous into the anterior chamber angle. Once lodged in the trabecular meshwork
in sufficient quantity, pigment can effectively create a blockade to aqueous outflow. This results in
elevated IOP with possible damage to the optic nerve--classic pigmentary glaucoma.
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Handbook of Ocular Disease Management - Pigment Dispersion Syndrome and Pigmentary Glaucoma
Recent studies using ultrasound biomicroscopy have shown distinct anatomical differences in the
angles of some patients with PDS and PG. In patients with PDS and PG, there is a posterior bowing
of the peripheral iris that precipitates the zonular touch. The term "reverse pupillary block" describes a
condition in which anterior chamber pressure intermittently exceeds that of the posterior chamber,
enhancing this backward displacement of the iris and resulting in further pigment liberation and IOP
spikes. The etiology is unclear, but it is thought that blinking in some patients results in this reverse
valve effect.
Management: Because PDS does not affect ocular health or vision, other than raising the risk for
PG, you should treat patients with PDS as glaucoma suspects and monitor them for IOP spikes and
optic nerve changes 3-4 times a year, with threshold visual fields and gonioscopy performed annually.
Patients with pigmentary glaucoma call for topical miotics as a first line of defense. Miotics are
preferable to beta-blockers or adrenergic agents because they have a dual effect; they not only lower
IOP, but also contract the pupil, pulling the peripheral iris away from the zonular fibers. Pilocarpine
solution 1% or 2% qid is an effective starting point; pilocarpine ointment 4% (Pilopine HS gel) once
daily at bedtime may work well as an alternative in younger patients.
If this regimen does not successfully control the IOP, additional agents such as beta-blockers, alpha-2
adrenergic agonists and topical carbonic anhydrase inhibitors may be necessary, either adjunctively
or alternatively, to achieve the target pressure. The use of prostaglandin-like medications in managing
PG is controversial. Conventional thinking dictates that these medications can increase the size of
melanosomes in some patients, which could increase blockage at the trabecular meshwork and
worsen the situation. However, the melanosomal enlargement occurs deep within the iris stroma and
is unlikely to affect aqueous outflow. Studies show that glaucoma resulting from pigment release can
be well managed by prostaglandins, and there appears to be no problems with outflow blockage from
increasing melanosomes size.1
Progressive, poorly responsive cases may require argon laser trabeculoplasty or filtering procedures.
More recently, clinicians have used laser peripheral iridotomy in patients with posterior iris bowing.
This is an attempt to reestablish a planar configuration to the angle and to equalize the pressure
between the anterior and posterior chambers.
Clinical Pearls:
●
PDS is a relatively benign condition while pigmentary glaucoma may lead to irreversible vision
loss if not detected early and managed accordingly.
●
As with any case of glaucoma, you must differentiate PG from other secondary glaucomas,
including exfoliative, uveitic and angle recession.
●
You must also recognize that PG is not typically a slow, insidious disease--often the onset and
progression are quite rapid. The "watch-and-wait" attitude that you might use with POAG is not
suitable with cases of PG. Prompt, aggressive therapy is indicated as soon as the diagnosis is
evident.
●
As patients with PG age, the altered configuration of the cataractous lens may resolve the irido-
zonular apposition and pigment release; the condition may then self-limit or "burn out" over
time.
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●
Due to gravity, pigment accumulation is greatest in the inferior angle and least in the superior
angle. If a patient presents with PDS or PG and the pigment accumulation is greater superiorly
than inferiorly, this "reversal" indicates a case that is "burned out" and almost resolved.
1. Konstas AG, Lake S, Maltezos AC, Holmes KT, Stewart WC. Twenty-four hour intraocular pressure
reduction with latanoprost compared with pilocarpine as third-line therapy in exfoliation glaucoma. Eye
2001 Feb;15(Pt 1):59-62.
Other reports in this section
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Pigment Dispersion Syndrome and Pigmentary Glaucoma
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Handbook of Ocular Disease Management - Primary Open Angle Glaucoma (POAG)
PRIMARY OPEN ANGLE GLAUCOMA (POAG)
SIGNS AND SYMPTOMS
Although early POAG patients are virtually asymptomatic, there are at
least three definitive signs: elevated intraocular pressure
(approximately 21mm Hg or more), enlargement of the optic cup and
repeatable field loss. Other possible signs include nerve fiber layer
dropout, notching of the neuroretinal rim at the inferior or superior
poles, and splinter hemorrhages adjacent to the optic disc.
PATHOPHYSIOLOGY
Despite decades of research and over two million diagnosed cases of open angle glaucoma in the U.S. alone,
much remains unknown about this disease. Elevated intraocular pressure almost certainly plays a significant
role, but the process is poorly understood. According to the mechanical theory of POAG, chronically elevated
IOP crimps the axons of retinal ganglion cells as they pass through the lamina cribrosa, eventually killing the
cells. The vascular theory suggests that, with elevated IOP, reduced blood flow to the optic nerve starves the
cells of oxygen and nutrients.
New research presented in 1996 offers another possible mechanism of ganglion cell death. Studies show that
some glaucoma patients exhibit elevated levels of the neurotransmitter glutamate within the vitreous. Ganglion
cells contain protein receptors that, when activated by glutamate, increase intracellular calcium to toxic levels,
killing the cells.
MANAGEMENT
Although several new IOP lowering drugs have been released in the past few years, beta-blockers continue to be
the mainstay of glaucoma therapy. The typical management plan is to set a target IOP at least 25 percent below
pre-treatment levels, and prescribe your beta-blocker of choice two or three times per day until the target is
reached.
The 19-year-old timolol (Timoptic) is the most commonly prescribed beta-blocker available, but others are also
noteworthy. Betimol from Ciba Vision Ophthalmics is a new, low-cost formulation of timolol that, unlike
Timoptic, cannot be surreptitiously replaced with a generic by the pharmacist.
A familiar but often overlooked beta-blocker that is gaining in prominence is betaxolol (Betoptic). This drug
selectively blocks beta-1 receptors, largely sparing beta-2 receptors in the lungs and thereby making it a safer
option for patients with some pulmonary conditions. Betoptic also has less likelihood of reducing blood flow
(and may, in fact, increase perfusion) to the optic nerve than other beta-blockers, has less propensity to reduce
the levels of HDL cholesterol in blood, and preserves the visual field equally or better than other beta-blockers,
even though its IOP reduction tends to be somewhat less. Finally, new research also shows that betaxolol
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Handbook of Ocular Disease Management - Primary Open Angle Glaucoma (POAG)
provides ganglion cells with at least some protection from calcium toxicity caused by glutamate binding.
Other unique beta-blockers include carteolol, which, like betaxolol, has less propensity to reduce HDL
cholesterol levels, and Timoptic-XE, which allows for once-a-day therapy.
New medications such as the prostaglandin analog latanoprost (Xalatan) and the topical carbonic anhydrase
inhibitor dorzolamide (Trusopt) offer alternative therapies, but beta-blockers have been the gold standard
against which all new pressure lowering medications are measured, and this is unlikely to change. In all
likelihood, beta-blockers will remain the first-line therapy of choice in POAG, and prostaglandin analogs will
supplant older second-line therapies. Xalatan is comparable in IOP lowering effect to Timoptic; its main side
effect is darkening of the pigment in light-colored irises.
Another new IOP lowering drug, the alpha-2 adrenergic agonist brimonidine (Alphagan), has not been proven
clinically superior to apraclonidine (Iopidine) although it is approved for chronic use whereas Iopidine 1% is
intended to control post-surgical pressure spikes and angle closure attacks. A lower concentration, Iopidine
0.5%, has been developed and approved for chronic care of POAG patients. It is likely that Alphagan and
Iopidine will equally share the alpha-2 adrenergic agonist market.
CLINICAL PEARLS
Prostaglandin analogs reduce IOP by increasing aqueous outflow through the uveoscleral pathway by dilating
the spaces between ciliary muscle bundles. However, miotics such as pilocarpine tighten these bundles by
contracting the iris dilator muscle, so these two medications are counter-effective. Discontinue any miotics prior
to adding Xalatan to the regimen.
To improve compliance for patients on multiple medications, it is helpful to identify the cap colors of each drug
being used (e.g., "Remember to use the one with the yellow cap twice a day and the blue one four times a day.")
Other Reports in This Section
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Primary Open Angle Glaucoma
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Handbook of Ocular Disease Management - Primary Open-Angle Glaucoma (POAG)
Primary Open-Angle Glaucoma (POAG)
Signs and Symptoms: Although early and moderate POAG patients are virtually asymptomatic,
there are definitive signs: progressive enlargement of the optic cup at the expense of the neuroretinal
rim (either diffusely or focally) and repeatable visual field loss. Other glaucomatous signs include
elevated intraocular pressure in many cases, nerve fiber layer (NFL) loss, notching of the neuroretinal
rim at the inferior or superior poles, advancing peripapillary atrophy and NFL hemorrhages emanating
from the optic disc.
Pathophysiology: Even today, much remains unknown about this disease. Elevated IOP almost
certainly plays a significant role, but the process is poorly understood. According to the mechanical
theory of POAG, chronically elevated IOP distorts the lamina cribrosa, crimping the axons of retinal
ganglion cells as they pass through the lamina cribrosa and eventually killing the cells. The vascular
theory suggests that with elevated IOP, reduced blood flow to the optic nerve starves the cells of
oxygen and nutrients.
More recent research suggests another mechanism of ganglion
cell death. Some glaucoma patients exhibit elevated levels of the
neurotransmitter glutamate within the vitreous. Ganglion cells
contain protein receptors that, when activated by glutamate,
increase intr acellular calcium to toxic levels, forming destructive
fig01.jpg (5755 bytes)
free radicals that kill the cells. This plays into the apoptotic theory
of glaucoma--a neurocellular process in which a retinal ganglion
cell will commit "suicide." Apoptosis is a normal cellular event
designed to ensure a healthy neurological system where non-
viable cells are removed. Glaucoma is an abnormal expression
of this normal process.
Advanced cupping and nerve fiber
layer defect in primary open angle
Excess glutamate accumulation--which may result from
glaucoma.
ischemia--may trigger apoptosis. Another possible inciting event:
the deprivation of vital neurotrophic nutrients for the retinal ganglion cells from the lateral geniculate
nucleus. The vital nutrient--brain derived neurotrophic factor (BDNF)--reaches the retinal ganglion
cells from the lateral geniculate nucleus via axoplasmic transport. Elevated IOP and ischemia disrupt
axoplasmic transport and deprive the retinal ganglion cells of this vital nutrient.
Management: Significant advances have been made in recent years in diagnostic devices for
glaucoma. A scanning laser ophthalmoscope (Heidelberg Retinal Tomograph II) can identify
abnormalities in optic disc morphology and compare them against a normative database,
documenting changes to the optic disc topography over time. A scanning laser polarimeter (GDx
Nerve Fiber Analyzer by Laser Diagnostic Technologies) can accurately identify changes in the retinal
nerve fiber layer. Here again, a normative database assigns statistical significance and can identify
abnormalities in the nerve fibers. Genetic testing (Ocugene) can identify patients with genetic
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Handbook of Ocular Disease Management - Primary Open-Angle Glaucoma (POAG)
characteristics of glaucoma and possibly predict the course of the disease.
Despite advances in diagnostic technology and new research into neuroprotection, the mainstay of
glaucoma treatment remains IOP reduction. Beta-blockers are still very popular medications and used
in many cases of POAG. Timoptic (timolol maleate, Merck) is the most commonly prescribed beta-
blocker, but others are also noteworthy.
Betoptic S (betaxolol 0.25% suspension, Alcon) selectively
blocks beta-1 receptors, largely sparing beta-2 receptors in the
lungs (making it a safer option for patients with certain pulmonary
conditions, though other classes of medication may ultimately be
safer for these patients). Other unique beta-blockers include
Ocupress (carteolol, Novartis)--which has less propensity than
fig01.jpg (5755 bytes)
other beta-blockers to elevate total cholesterol levels and reduce
HDL cholesterol levels--and Timoptic-XE (timolol maleate,
Merck), which allows for once-a-day therapy.
Alpha-adrenergic medications advanced with the development of
Alphagan (brimonidine 0.2%, Allergan), a selective alpha-2
Endstage primary open-angle
adrenergic agonist. This medication has an excellent safety
glaucoma.
profile and IOP-lowering potential similar to beta-blockers. While
clinicians have frequently prescribed Alphagan bid, clinical studies show that it should be prescribed
tid, especially when used as monotherapy. Otherwise, IOP control could be lost at times throughout
the day. The most common adverse effect has been allergic reactions. A new formulation, Alphagan
P (brimonidine 0.15% in Purite), has reduced the incidence of local allergic reactions by 41%.1
Topical carbonic anhydrase inhibitors such as Trusopt (dorzolamide, Merck) and Azopt (brinzolamide,
Alcon) have been successful in lowering the IOP in many patients. However, few clinicians use these
medications as first-line therapy. Cosopt (Merck), which combines timolol 0.5% with dorzolamide, can
be effective when a single agent fails to control IOP.
IOP control was revolutionized with the development of prostaglandin analogs and prostaglandin-like
medications. Xalatan (latanoprost, Pharmacia) has enjoyed considerable success, offering
outstanding IOP lowering, long-term control, and minimal local and systemic effects. Rescula
(unoprostone, Novartis), actually a docosanoid, has a similar safety profile to Xalatan, though its IOP-
lowering is not as great and it requires bid dosing.
More recently developed is Lumigan (bimatoprost, Allergan). Like Xalatan, this medication increases
uveoscleral outflow of aqueous and has outstanding IOP-lowering ability. The medication is well
tolerated systemically, hyperemia being the main adverse effect.
Another new prostaglandin analog, Travatan (travoprost, Alcon) apparently has a greater IOP-
lowering potential in patients of African descent. It, too, is well tolerated systemically and ocularly.
Travatan has been shown to be more effective than Timoptic in IOP reduction.2-3
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Handbook of Ocular Disease Management - Primary Open-Angle Glaucoma (POAG)
Clinical Pearls:
●
Glaucoma is a long-term disease. Accumulate the necessary information so that you can
diagnose with confidence. Do not to rush to a diagnosis. It typically is not necessary to
diagnose the disease and start treatment at the patient's initial presentation.
●
A single IOP measurement does not accurately represent the patient's true status, but is
merely a snapshot pressure at that moment. Before making a diagnosis or initiating treatment,
take repeated IOP measurements at different times on different days so that you have a more
accurate picture of the patient's IOP "baseline range."
●
While scanning lasers have not supplanted visual fields in the diagnosis and management of
glaucoma, they provide useful information on optic nerve head and nerve fiber layer structure.
●
Prostaglandins and prostaglandin-like medications are not FDA-approved as first-line therapy
due to the possibility of inducing ocular inflammation and iris color changes. Yet many
clinicians use them as first-line therapy.
1. Katz LJ. Twelve-month evaluation of brimonidine-purite versus brimonidine in patients with glaucoma or
ocular hypertension. J Glaucoma 2002 Apr;11(2):119-26.
2. Fellman RL, Sullivan EK, Ratliff M, et al. Comparison of travoprost 0.0015% and 0.004% with timolol
0.5% in patients with elevated intraocular pressure: a 6-month, masked, multicenter trial. Ophthalmology
2002 May;109(5):998-1008.
3. Goldberg I, Cunha-Vaz J, Jakobsen JE, et al. Comparison of topical travoprost eye drops given once
daily and timolol 0.5% given twice daily in patients with open-angle glaucoma or ocular hypertension. J
Glaucoma 2001 Oct;10(5):414-22.
Other reports in this section
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Primary Open-Angle Glaucoma
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Handbook of Ocular Disease Management - Treating POAG: How Low Should IOP Go?
Treating POAG: How Low Should IOP Go?
Choosing a target intraocular pressure has always been an inexact science. The greater and more
consistent the reduction in IOP, the greater the reduction of subsequent nerve damage. The target
pressure is different for each patient and there is no clearly, scientifically defined IOP level below
which an eye is safe from pressure-related damage. Some clinicians set a target at a percentage
reduction from baseline while others use more complicated formulas that have no proven validity.
The results of the Advanced Glaucoma Intervention Study (AGIS) have proven that the popular
thinking about low IOP preventing damage is correct.1 In this study, patients with advanced glaucoma
who had failed medically were randomized into surgical groups employing a preset algorithm of argon
laser trabeculoplasty and trabeculectomy. A side arm of the study examined the role of IOP-reduction
in preventing further damage.
Patients were grouped into categories based upon the percentage of study visits where the IOP was
below 18mm Hg. Patients who presented with 100% of study visits below 18mm Hg had, on average,
little deterioration of their visual fields over six years. The patients in this group had an average IOP of
12.3mm Hg. Patients who had fewer than 50% of study visits in which IOP was below 18mm Hg had
much more significant visual field deterioration. These patients had an average IOP of 20.2mm Hg.
The AGIS study clearly shows that low post-intervention IOP is associated with a positive outcome
(visual fields are better preserved). This is one well-conducted scientific study that definitively shows
that lowering IOP is beneficial in glaucoma management. However, must the study results be
matched in all glaucoma patients? Should we insist on an IOP of 14mm Hg or less on every patient?
While this research seems impeccable and the results credible,
clinicians need to understand how to integrate this information into clinical practice.
While patients who had IOP < 14mm Hg (average 12.3mm Hg and all study visits under 18mm Hg)
did the best, remember that the patients in this study had advanced glaucoma and already had failed
on medical therapy. Not all patients have advanced glaucoma; hence an IOP under 14mm Hg may be
excessive. As we force the IOP lower and lower, so we decrease the patient's quality of life in terms
of expense, adverse therapeutic effects and other unforeseen consequences. You still must consider
many factors when determining a patient-specific goal for IOP range.
While the below-14mm Hg group experienced visual field changes that were nearly zero, this
represents an average change which incorporates patients who actually had improvement in their
visual fields throughout the study. This means that there were also patients in this low-IOP group who
did experience visual field deterioration. Please be aware that an IOP of 12-14mm Hg does not
guarantee that the patient will not experience further glaucomatous losses.
The significance of this study is that, for patients with advanced glaucoma, attaining low IOPs (in the
12-14mm Hg range) is an indication that we are likely benefiting the patients. Remember that
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Handbook of Ocular Disease Management - Treating POAG: How Low Should IOP Go?
maintaining a steady diurnal IOP curve is just as important to maintaining optic nerve health as is
attaining low IOP. Fortunately the newest class of glaucoma medications, the prostaglandin analogs,
affords us the ability to medically reach lower IOP than ever before, as well as stabilize the IOP
diurnal curve.
1. The AGIS investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship
between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000; 130: 429-
40.
Other reports in this section
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Treating POAG: How Low Should IOP Go?
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Handbook of Ocular Disease Management - Pseudoexfoliation and Pseudoexfoliative Glaucoma
PSEUDOEXFOLIATION SYNDROME AND
PSEUDOEXFOLIATIVE GLAUCOMA
SIGNS AND SYMPTOMS
Patients with pseudoexfoliation syndrome remain asymptomatic until an
advanced glaucoma develops. The condition is most common in the
sixth to eighth decade, with actual glaucoma developing later in this age
range. There is no racial, sexual or geographic predilection. Typically,
pseudoexfoliation syndrome begins unilaterally, but becomes bilateral
within about seven years.
The patient presents with a fine, flaky material on the anterior lens capsule at the pupillary margin. Over time,
this coalesces into a characteristic "bulls-eye" pattern seen in pseudoexfoliation. There is often increased
transillumination of the iris at the pupillary margin and there may be pigment granules on the endothelium and
iris surface. Within the angle, there may be observable pigment or clear flaky material. Initially, intraocular
pressure is unaffected; however, elevated IOP develops in up to 80 percent of patients. In these cases,
glaucomatous cupping and visual field loss may ensue.
PATHOPHYSIOLOGY
Due to accumulation of abnormal basement membrane material at the pupillary margin, there is increased
apposition with the iris and subsequent erosion of iris pigment as the pupil dilates and constricts. This leads to
increased iris transillumination and deposition of pigment granules on the endothelium, iris surface and
trabecular meshwork similar to pigment dispersion syndrome. Because this condition involves deposition of
material on the anterior lens capsule, and not flaking-off of the lens capsule, lensectomy is not a remedy. In fact,
some have observed exfoliative material deposits on intraocular lens implants.
The development of glaucoma typically occurs due to a buildup within the trabecular meshwork of pigment
granules and pseudoexfoliative material. Patients develop a secondary open angle glaucoma. However, studies
have identified patients with increased IOP but no decrease in aqueous outflow. In these cases, the glaucomatous
mechanism is unknown.
MANAGEMENT
Pseudoexfoliation syndrome without a pressure rise requires only periodic monitoring of IOPs, discs and visual
fields. When first diagnosing pseudoexfoliation syndrome, perform automated visual fields to look for
preexisting field loss since pseudoexfoliative glaucoma undergoes periods of exacerbation and remission.
Treat pseudoexfoliative glaucoma in the same manner as primary open angle glaucoma. Use topical beta-
blockers, topical carbonic anhydrase inhibitors, prostaglandin analogs and alpha adrenergic agonists if not
systemically contraindicated. However, the IOP level in pseudoexfoliative glaucoma is typically higher than in
POAG and is more difficult to temporize. Laser trabeculoplasty and filtration surgery are often employed earlier
than in POAG.
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Handbook of Ocular Disease Management - Pseudoexfoliation and Pseudoexfoliative Glaucoma
CLINICAL PEARLS
●
An initially normal IOP measurement does not preclude prior IOP elevation with subsequent field loss
and disc damage. Remember that pseudoexfoliative glaucoma undergoes periods of exacerbation and
remission. Serial photographs and automated visual fields are more appropriate for managing this
condition than IOP measurements, since the patient may experience progression yet manifest normal
IOP if measured during remission.
●
Argon laser trabeculoplasty and filtration surgery are more effective in controlling IOP in cases of
pseudoexfoliative syndrome than in POAG.
Other Reports in This Section
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Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
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Handbook of Ocular Disease Management - Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
Signs and Symptoms: A patient with pseudoexfoliation
syndrome remains asymptomatic until an advanced glaucoma
develops. The condition is most common in those in their 50s to
70s; glaucoma develops later in this age range.
Pseudoexfoliation syndrome begins unilaterally but becomes
fig01.jpg (5755 bytes)
bilateral within about seven years.
The patient will present with a fine, flaky material on the anterior
lens capsule at the pupillary margin. Over time, this will coalesce
into a characteristic "bulls-eye" pattern. There is often increased
Pseudoexfoliative material on
transillumination of the iris at the pupillary margin, and there may
anterior lens capsule in pseudo-
be pigment granules on the endothelium and iris surface. Within exfoliation syndrome and pseudo-
exfoliative glaucoma.
the angle there will be heavy pigment reminiscent of pigment
dispersion syndrome, and you may see a clear, flaky material.
Initially, IOP is unaffected, but later rises in up to 40% of patients.1 In these cases, characteristic
glaucomatous cupping and visual field loss may ensue.
Pathophysiology: We don't know conclusively the nature of the material deposited in the anterior
chamber. Most researchers agree that it represents abnormal basement membrane that structures
within the anterior chamber secreted and deposited on the anterior lens capsule, iris surface and
trabecular meshwork. Because material accumulates at the pupillary margin, there is increased
apposition with the iris and subsequent erosion of iris pigment as the pupil dilates and constricts. This
leads to increased iris transillumination and deposition of pigment granules on the endothelium, iris
surface and trabecular meshwork. Because this involves deposition of material on the anterior lens
capsule, and not flaking-off of the lens capsule, lensectomy is not a cure.
Glaucoma typically develops due to a build-up within the trabecular meshwork of pigment granules
and pseudoexfoliative material. Patients develop a secondary open-angle glaucoma. However,
studies have identified patients with increased IOP but no decrease in facility of aqueous outflow.
Management: Pseudoexfoliation syndrome without an IOP rise requires only periodic monitoring of
IOP, discs and visual fields. When first diagnosing pseudoexfoliation syndrome, do automated visual
fields to look for preexisting field loss; pseudoexfoliative glaucoma waxes and wanes.
Treat pseudoexfoliative glaucoma the same way you would POAG--with topical beta-blockers,
carbonic anhydrase inhibitors, prostaglandin analogs and alpha-adrenergic agonists. The IOP level in
pseudoexfoliative glaucoma is typically higher than it is in POAG and is more difficult to lower. Laser
trabeculoplasty and filtration surgery are often indicated earlier with pseudoexfoliative glaucoma than
in POAG.
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Handbook of Ocular Disease Management - Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
Miotics can effectively manage pseudoexfoliative glaucoma. Pupil constriction reduces the rubbing of
the posterior iris against the pseudoexfoliative material, thus reducing the amount of pigment and
material released into the aqueous convection current.
Clinical Pearls:
●
An initially normal IOP measurement does not preclude the possibility that the patient
previously had elevated IOP with subsequent field loss and disc damage.
●
Serial photographs and automated visual fields are more appropriate than IOP measurements
for managing this condition. The patient may have progression yet manifest normal IOP in the
office during a trough.
●
ALT and filtration surgery are more effective in controlling IOP in cases of pseudoexfoliative
syndrome than in POAG.
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Patients with pseudoexfoliative glaucoma have wider fluctuations in IOP throughout the day
than do patients with POAG. The highest IOPs in patients with pseudoexfoliative glaucoma
occur outside of normal office hours.
1. Henry JC, Krupin T, Schmitt M, et al. Long term follow-up of pseudoexfoliation and the development of
elevated intraocular pressure. Ophthalmol 1987; 94: 545-9
Other reports in this section
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Handbook of Ocular Disease Management - Understanding Nerve Fiber Layer Analysis
Understanding Nerve Fiber Layer Analysis
When researchers discovered that a great
amount of retinal ganglion cells are lost prior to
the development of visual field defects, they
studied the retinal nerve fiber layer, initially with
an ophthalmoscope. However, just as
automated perimetry has replaced tangent
screens, new technology has been developed
to study the retinal nerve fiber layer.
Laser Diagnostic Technology introduced the
GDx nerve fiber layer analyzer (GDx NFA) to
fig01.jpg (5755 bytes)
accurately measure the retinal nerve fiber layer.
This device is a scanning-laser polarimeter.
Laser light double-passes the retinal nerve fiber
layer (NFL) and splits into two parallel rays by
the birefringent fibers. The two rays travel at
different speeds and this difference (called
retardation) directly correlates to the thickness
of the nerve fiber layer.
This test is completely objective and takes
about 10 minutes to complete, though it makes
The GDx Access nerve fiber layer analyzer.
the actual measurements in less than one
second. It works best on undilated pupils and
can work quite well through cataracts up to 20/60. A normative database compares the patient's
measurements to those of normal patients of the same age, sex, and race.
Key Points in Interpretation
In each analysis, the 1,500 thickest points in
superior and inferior quadrants are identified as
well as the 1,500 median points within the nasal
and temporal quadrants. The GDx NFA bases
its calculations on parameters which best
differentiate normal patients from those with
glaucoma. These parameters include symmetry
of various quadrant ratios, nerve fiber layer
area, nerve fiber layer thickness above blood
vessels, absolute thickness of all measured
points, and total volume of nerve fiber layer.
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Handbook of Ocular Disease Management - Understanding Nerve Fiber Layer Analysis
• Color Image. Color has been artificially added
to this image of the optic nerve head and
peripapillary retina to assist the operator in
observing the nerve head and appreciating the
quality of the scan performed.
• Thickness (Polarization) Map. This is a map of
measured points creating a color-coded image
fig01.jpg (5755 bytes)
to indicate NFL thickness. Bright colors (red and
yellow) are associated with thicker areas,
signifying healthy NFL. Dark colors (blue) are
associated with thinner areas, indicating less
healthy NFL.
• TSNIT (Double Hump) Graph. The right eye is
depicted in blue and left in yellow. This displays
the normal range and the patient's NFL
A serial analysis printout.
thickness from the 200 points along the ellipse.
It is a quick, easy look at how the patient
compares with normal.
• Symmetry Analysis. This is an overlay of O.D. and O.S. TSNIT graphs. It allows for easy
comparison of symmetry between the two eyes.
Nerve Fiber Analysis
These values compare the patient's NFL thickness values to an age- and race-matched population of
normal patients, and evaluate a series of ratios, averages and other parameters. Any parameter
statistically eva luated as "borderline" or "outside normal" indicates that the patient does not match
normative values. No single parameter is more or less sensitive to detecting glaucoma. However,
these parameters do bear some explanation:
• The Number. A neural network within
the GDx analyzes more than 200
parameters from the image. It then
assigns a number between zero and
100 (zero means normal and 100
means glaucoma). This indicates the
likelihood that a patient has glaucoma.
As the number is still experimental, it
does not have a color to indicate
significance or deviation from normal.
• Symmetry. This represents the ratio
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Handbook of Ocular Disease Management - Understanding Nerve Fiber Layer Analysis
of the average of the 1,500 thickest
points in the superior quadrant over the
average of the 1,500 thickest points in
the inferior quadrant. The closer this
number is to 1.0, the more symmetry is
present, and the more normal the
patient.
fig01.jpg (5755 bytes)
• Max Modulation. This is an indication
of the difference between the thickest
part of the NFL and the thinnest part.
The higher the number, the greater the
difference. In a normal eye in which the
superior and inferior region is thicker
than the nasal or temporal region, the
modulation number will usually be
greater than 1.0. Lower numbers are
associated with loss of thickness of the
NFL and are characteristic of glaucoma.
Birefringence can occur in an analysis from ocular structures other than the nerve fiber layer,
introducing artifacts into the analysis. A new development in the form of a Custom Corneal
Compensator may address the difficulty.
While early studies showed a high sensitivity and specificity of the GDx NFA for glaucoma, other
studies have questioned the device's ability to correctly identify early cases. There is no single
parameter (or even combination) that will identify the presence of glaucoma in every case. While the
device can give an accurate representation of the status of the nerve fiber layer, it should not form the
sole basis for diagnosis.
The authors have no direct financial interest in Laser Diagnostic Technology or the GDx nerve fiber
layer analyzer.
Other reports in this section
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Understanding Nerve Fiber Layer Analysis
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Handbook of Ocular Disease Management - Uveitic Glaucoma & Glaucomatocyclitic Crisis
UVEITIC GLAUCOMA & GLAUCOMATOCYCLITIC CRISIS
SIGNS AND SYMPTOMS
Patients with uveitic glaucoma will present with a unilateral red,
painful, photophobic, lacrimating eye. Acuity will be moderately
decreased. There will be corneal edema and folds in Descemet's
membrane, but the epithelium should be intact. There will be a profuse
anterior chamber reaction, possibly with hypopyon. There are
frequently posterior synechiae. There will be injection of the
conjunctival and episcleral vessels. The angle may be closed with
peripheral anterior synechiae (PAS). Intraocular pressure (IOP) may
range from 30 to 80mm Hg.
The patient with glaucomatocyclitic crisis will present with a recurrent, unilateral red eye with very mild
discomfort, or possibly no discomfort at all. Acuity will be mildly reduced; this is often the chief complaint. The
cornea will be mildly edematous, but the anterior chamber will be remarkably clear. Often, the only signs of
anterior chamber inflammation will be a rare cell or two in the chamber or, more commonly, a few keratic
precipitates on the endothelium. Intraocular pressure can range from 30 to 70mm Hg, but the patient will not be
in acute distress.
PATHOPHYSIOLOGY
In uveitic glaucoma the patient first develops uveitis, either due to trauma, systemic disease or idiopathically.
The ensuing inflammation results in a rise in IOP through several mechanisms.
Often, the inflammatory cells physically block the trabecular meshwork, decreasing aqueous outflow, with the
angle remaining open. Occasionally, the inflammatory cells and fibrous protein will form a connective bridge
between the peripheral iris and cornea, pulling these structures into apposition, and resulting in an angle closure
with PAS formation.
Because the inflammatory cells and protein in the anterior chamber form adhesions between the posterior iris
and anterior lens, posterior synechiae commonly form. This will lead to iris bombé, secondary angle closure and
peripheral anterior synechiae formation. There may also be a combination of mechanisms that increases IOP.
Untreated, the patient will eventually experience glaucomatous optic atrophy, or possibly central retinal artery
occlusion.
In glaucomatocyclitic crisis, there is an idiopathic inflammation of the trabecular meshwork that reduces this
structure's ability to actively drain aqueous. Due to prostaglandin release, it is theorized that there may also be a
concurrent overproduction of aqueous. Despite the elevated IOP, this condition is only mildly symptomatic, and
is usually self-limiting. However, the recurrent nature of the attacks predisposes the patient to developing
glaucomatous optic atrophy.
MANAGEMENT
Successful management of uveitic glaucoma involves prompt and aggressive measures. In any inflammatory
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Handbook of Ocular Disease Management - Uveitic Glaucoma & Glaucomatocyclitic Crisis
glaucoma, you must treat the inflammation first and the IOP secondarily. Initiate strong cycloplegia in the form
of atropine 1% BID immediately to put the uveal tissue at rest and begin healing. Have the patient use a steroid
such as Vexol (rimexolone), Pred Forte (prednisolone acetate) or fluorometholone acetate (Flarex, Eflone) every
15 minutes for the first several hours, then taper to every hour.
If any posterior synechiae have formed, prescribe phenylephrine 10% BID. Quelling the inflammation will
temporize the IOP rise. To further reduce the IOP, use a topical beta-blocker BID or the topical carbonic
anhydrase inhibitor Trusopt TID, provided there are no medical contraindications to any of these drugs. Avoid
pilocarpine and other miotics in these patients. Follow the patient every 24 hours and gradually taper the
medications as the condition improves.
Management of glaucomatocyclitic crisis is nearly identical to that described above for uveitic glaucoma, with
the following two exceptions:
(1) It is acceptable to use a slightly weaker cycloplegic such as scopolamine (hyoscine 0.25%) or homatropine
5% BID.
(2) The patient should instill a topical steroid hourly rather than every 15 minutes.
CLINICAL PEARLS
●
Avoid pilocarpine and other miotics in inflammatory glaucoma. Miotics will induce ciliary spasm and
increase inflammation, fostering both posterior and peripheral anterior synechiae. We have seen many
cases of inflammatory glaucoma improperly treated with pilocarpine; all patients worsened considerably
and one ultimately resulted in enucleation.
●
Steroids are absolutely necessary to manage inflammatory glaucoma. However, practitioners tend to be
hesitant to prescribe steroids for patients with elevated IOP for fear of a concomitant steroid-induced
pressure rise. One must realize that steroids will not increase IOP for at least two weeks, and this
pressure rise only occurs in one-third of the population. In fact, steroids will actually reduce IOP by
quelling the inflammation. Withholding steroids in inflammatory glaucoma is extreme mismanagement.
●
Strong cycloplegia is necessary in managing uveitic glaucoma. The use of tropicamide, cyclogel or other
weak cycloplegic agents is considered poor management.
●
Avoid the prostaglandin analog latanoprost (Xalatan) since, as in any inflammatory condition, there will
already be copious amounts of prostaglandins in the anterior chamber and Xalatan will not provide any
benefit.
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Remember: treat the inflammation first and the IOP secondarily!
Other Reports in This Section
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Handbook of Ocular Disease Management - Uveitic Glaucoma & Glaucomatocyclitic Crisis
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Handbook of Ocular Disease Management
PHACOMORPHIC GLAUCOMA
Signs and Symptoms
Patients with phacomorphic glaucoma are typically elderly, female, and often of small stature.
Frequently, they are hyperopic with a nanophthalmic eye. By definition an advanced, intumescent
cataract will be present in the affected eye. Visual acuity is poor, often well below 20/400. There will
be a shallow anterior chamber. In eyes with markedly asymmetric cataract formation, anterior
chamber depth may be accordingly disparate. Often, patients will present with acute onset of ocular
redness and pain with an edematous cornea and elevated IOP. Gonioscopically, during the acute
attack, there will be corneal edema, and no anterior chamber angle structures will be visible.
Occasionally, there may be a precipitating incident such as pharmacological pupil dilation.1-3
Pathophysiology
Phacomorphic glaucoma is a patho-logic rise in IOP precipitated by the shape of the lens. That is, the
lens becomes intumescent and thickened through the process of cataractogenesis. This can cause a
relative pupil block with secondary angle closure with all of the attendant signs and symptoms of an
acute angle closure attack. Further, the swelling of the lens may press upon the iris and ciliary body,
forcing them anteriorly and shallowing the anterior chamber. Thus, there can be an acute angle
closure attack that may not respond to laser peripheral iridotomy (LPI).
Management
Medical therapy is used to reverse the process and acutely lower the IOP. Beta-blockers, alpha-2
adrenergic agonists, topical corticosteroids, topical or oral carbonic anhydrase inhibitors, and oral
hyperosmotics may all be systematically employed. Superior IOP control and shortening the duration
of the attack preoperatively is essential in improving the final visual outcome.4
In cases where pupil block precipitates an angle closure, LPI is indicated following medical treatment
to attempt to relieve the resultant aqueous congestion and IOP rise.5 This is especially true when
relative pupil block is the main pathogenesis. In cases in which pupil block only partially contributes to
the angle closure, argon laser peripheral iridoplasty can reverse the apposition and alleviate the
condition.
Cataract extraction will ultimately relieve the condition. Extracapsular cataract extraction, either with
or without secondary lens implantation, remains the most common procedure to correct
phacomorphic glaucoma.6-8 There often is a poor visual outcome secondary to both surgical
complications as well as the lens induced glaucoma.9 This is especially true for patients over 60 years
and those in whom the glaucoma has persisted beyond five days.6
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Handbook of Ocular Disease Management
Clinical Pearls
●
While acute primary angle closure is typically symmetrical, phacomorphic glaucoma is not. Be
aware of a possibility of a narrow angle and shallow chamber in patients with advanced,
unilateral cataract.
●
Long-term miotic usage in patients with mature cataracts may predispose the patient to
phacomorphic glaucoma.
●
Patients with POAG may develop angle closure and phacomorphic glaucoma with continued
cataract development. Perform gonioscopy at least annually on all glaucoma patients.
1. Abramson DH, Franzen LA, Coleman DJ. Pilocarpine in the presbyope: Demonstartion of an effect on the
anterior chamber and lens thickness. Arch Ophthalmol 1973;89:100-2.
2. Gorin G. Angle closure glaucoma induced by miotics. Am J Ophthalmol 1966;62:1063-6.
3. Gayton JL, Ledford JK. Angle closure glaucoma following a combined blepharoplasty and ectropion repair.
Ophthal Plast Reconstr Surg. 1992;8(3):176-7.
4. Das JC, Chaudhuri Z, Bhomaj S, et al. Combined extracapsular cataract extraction with Ahmed glaucoma
valve implantation in phacomorphic glaucoma. Indian J Ophthalmol. 2002;50(1):25-8.
5. Tomey KF, al-Rajhi AA. Neodymium:YAG laser iridotomy in the initial management of phacomorphic
glaucoma. Ophthalmology. 1992;99(5):660-5.
6. Prajna NV, Ramakrishnan R, Krishnadas R, et al. Lens induced glaucomas--visual results and risk factors
for final visual acuity. Indian J Ophthalmol. 1996;44(3):149-55.
7. McKibbin M, Gupta A, Atkins AD. Cataract extraction and intraocular lens implantation in eyes with
phacomorphic or phacolytic glaucoma. J Cataract Refract Surg. 1996;22(5):633-6.
8. Rao SK, Padmanabhan P. Capsulorhexis in eyes with phacomorphic glaucoma. J Cataract Refract Surg.
1998;24(7):882-4.
9. Lim TH, Tan DT, Fu ER. Advanced cataract in Singapore--its prognosis and complications. Ann Acad Med
Singapore. 1993;22(6):891-4.
Other reports in this section
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Handbook of Ocular Disease Management
PHACOLYTIC GLAUCOMA
Signs and symptoms
The patient with phacolytic glaucoma is typically elderly with a history of progressively worsening vision from pre-existing cataracts. Vision typically is reduced to light perception
range, but the patient may have no light perception due to a hypermature cataract and the glaucomatous process.1 There may be movement of the lens as the patient's eye moves
(phacodonesis), indicating a loss of zonular support. The patient will experience ocular pain, sometimes quite severe. There will be anterior segment inflammation with an anterior
chamber reaction. A hypermature lens is invariably present. The intumescence of the lens prevents observation of the fundus ophthalmoscopically. Intraocular pressure is elevated
and asymmetric. Due to the types of inflammatory cells present, development of synechiae is uncommon.
Pathophysiology
Internal lens proteins gain access to the anterior chamber through the phacolytic process involving the hypermature cataract. There is liquefaction of the lens nucleus and cortex,
and attenuation of the capsule with the release of lens proteins into the anterior chamber. While the lens proteins are the host's own body tissue, they have never been exposed to
the anterior chamber due to their envelo pment by the lens capsule. Thus, the body detects these lens proteins as foreign and antigenic. Subsequently, an inflammatory reaction
ensues with a lens-induced uveitis.
Ultrastructural study of aqueous and vitreous aspirates shows lenticular fragments and macrophages with lipofuscin granules and phagocytic vacuoles containing lens proteins.2
Numerous macrophages having phagocytized degenerated lens material (phacolytic cells) can be found in the anterior chamber, and free-floating degenerated lens material is also
conspicuous.3 These constituents mechanically produce trabecular obstruction and dysfunction with subsequent rise in IOP.
Management
The first step in management involves quieting the acute inflammatory reaction and ameliorating the elevated IOP. Topical cortico-steroids are
indicated just as they would be for any anterior uveitis. Cycloplegics are also indicated. The choice should be dictated by the severity of the
uveitic response and the patient's degree of discomfort. Typically, homatropine and scopolamine are adequate choices. One caveat: In some
cases of phacolytic glaucoma, there may be loss of zonular support to the lens, indicated by phacodonesis. In these cases where there is poor
zonular support, cycloplegia with attendant pupil dilation may result in anterior dislocation of the lens, possibly into the anterior chamber. This
complication should be anticipated in these cases. Cycloplegia may need to be avoided if immediate surgical management is not available to
address this possible complication.
Secondary glaucoma accompanying phacolysis is often improved by the reduction in inflammation with topical steroid therapy. However, if
additional pressure reduction is necessary, aqueous suppressants are advocated, provided there are no systemic contraindications. How-ever,
miotics and prostaglandins should be avoided due to their propensity to aggravate the disease.
Phacolytic lens with inferior
subluxation.
In most cases, it is necessary to remove the antigenic lens in order to fully manage phacolytic glaucoma. Commonly, extracapsular and even
intracapsular cataract extraction are used to remove the antigenic lens. Either anterior or posterior chamber intraocular lens implantation can be
an option.4
In cases of long duration prior to surgery, trabeculectomy may additionally be needed in order to control IOP.5 Removal of the antigenic lens and
control of the glaucoma should be done quickly. One study found that patients over 60 years and in whom the glaucoma was present for more
than five days had a significantly higher risk of poor visual outcome post-op.6
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Handbook of Ocular Disease Management
The addition of trabeculectomy to cataract extraction is typically unnecessary in the control of IOP in patients with phacolytic glaucoma operated
on within two to three weeks of the onset of symptoms. Light perception without projection is not a contraindication for cataract surgery in
phacolytic glaucoma.7
Clinical Pearls
●
Phacolytic glaucoma develops only in eyes with hypermature cataracts. Vision typically ranges from finger counting to light perception. If
vision is better than 20/400, consider another cause.
●
Be careful to assess lens zonular integrity before employing a cycloplegic in phacolytic glaucoma.
●
Do not let elevated IOP prevent the use of steroids. The benefits of inflammation control in phacolytic glaucoma greatly outweigh the
potential risks of steroid-induced pressure elevation.
Phacolytic lens with secondary
glaucoma.
1. Podhorecki J, Munir A. Result of operations for hyper-mature cataract complicated with phacolytic glaucoma. Klin Oczna. 2002;104(5-6):350-3.
2. Filipe JC, Palmares J, Delgado L, et al. Phacolytic glaucoma and lens-induced uveitis. Int Ophthalmol. 1993;17(5):289-93.
3. Ueno H, Tamai A, Iyota K, et al. Electron microscopic observation of the cells floating in the anterior chamber in a case of phacolytic glaucoma. Jpn J Ophthalmol. 1989;33(1):103-13.
4. Singh G, Kaur J, Mall S. Phacolytic glaucoma--its treatment by planned extracapsular cataract extraction with posterior chamber intraocular lens implantation. Indian J Ophthalmol. 1994;42
(3):145-7.
5. Braganza A, Thomas R, George T, et al. Management of phacolytic glaucoma: experience of 135 cases. Indian J Ophthalmol. 1998;46(3):139-43.
6. Prajna NV, Ramakrishnan R, Krishnadas R, et al. Lens induced glaucomas--visual results and risk factors for final visual acuity. Indian J Ophthalmol. 1996;44(3):149-55.
7. Mandal AK, Gothwal VK. Intraocular pressure control and visual outcome in patients with phacolytic glaucoma managed by extracapsular cataract extraction with or without posterior chamber
intraocular lens implantation. Ophthalmic Surg Lasers. 1998;29(11):880-9.
Other reports in this section
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Handbook of Ocular Disease Management
IRIDOCORNEAL ENDOTHELIAL SYNDROMES (ICE)
Signs and Symptoms
The patient with ICE syndrome is typically a younger female. It is most common in Caucasians, and there typically is no family history of this disease. It is most commonly a unilateral
phenomenon, but bilateral cases have been documented.1 It tends to manifest in early to middle adulthood.2 Common findings include a beaten bronze appearance to the corneal
endothelium, corneal edema, iris atrophy and hole formation, corectopia, prominent iris nevus, and peripheral anterior synechiae with progressive angle closure and secondary
closed-angle glaucoma. Vision may be unaffected or may be reduced due to endotheliopathy or glaucoma. The patient may occasionally complain of monocular diplopia secondary
to an exposed area of full thickness iris atrophy creating another entrance for light to enter the eye (polycoria).
Pathophysiology
The ICE syndromes represent a continuum of disease involving three distinct entities: essential iris atrophy, Chandler syndrome, and Cogan-
Reese (iris nevus) syndrome. Essential iris atrophy is characterized by progressive iris atrophy and hole formation, corectopia, and marked
peripheral anterior synechiae. The iris and pupil are pulled in the direction of the peripheral anterior syn-echiae. Chandler syndrome, the more
common of the three, manifests greater corneal changes and edema but fewer iris abnormalities. Cogan-Reese syndrome presents with iris
atrophy, corneal endotheliopathy, corneal edema, and prominent iris nevi. Patients with Chandler's syndrome typically have worse corneal
edema than the rest of the group, while secondary glaucoma is more severe in the other syndromes.3
All the ICE syndromes share a common underlying pathophysiology and can all be considered to be primary proliferative endothelial
degenerations.4 The corneal endo-thelium has a fine beaten-silver appearance. This, along with ensuing corneal edema, is a cause of vision
reduction in these patients. The endothelium is most affected in essential iris atrophy. Some endo-thelial changes such as migration and
reparative processes are identifiable, as is the presence of cell necrosis and chronic inflammation.5 It appears that the endothelial cells undergo
Corectopia in essential iris atrophy.
a metaplastic transformation into "epithelial-like" cells that migrate in a membrane form over the anterior chamber angle to the iris.6 Subsequent
contraction of the membrane pulls the iris toward the cornea with a chronic progressive synechial closure of the angle. This can result in
secondary angle closure without pupil block. The cellular membrane may also cause aqueous outflow blockage in the absence of peripheral
anterior synechiae.
Management
Management of ICE syndromes is case specific and should be dictated by the degree of corneal edema and severity of the secondary
glaucoma. Topical aqueous suppressants are the medical mainstay for management of glaucoma secondary to ICE syndromes. Medications
that stimulate aqueous outflow are typically less effective and should not be used. Also, laser trabeculoplasty is not seen as effective. In severe
cases, trabeculectomy may be necessary, though there is a risk of closure of the sclerotomy site by the abnormal membranes, with subsequent
surgeries required.7,8 Glaucoma surgical implant devices may be necessary for this reason. Despite adequate IOP control, corneal edema may
persist due to the endotheliopathy. In these cases, penetrating keratoplasty may be necessary to restore vision, though this procedure will not
affect abnormalities in the iris or anterior chamber angle.9
Clinical Pearls
Peripheral anterior synechiae in
essential iris atrophy.
●
Essential iris atrophy, Chandler's syndrome, and Cogan-Reese syndrome are all in the same clinical disease spectrum of ICE syndromes
●
Progression is unpredictable, and many patients have a good outcome.
●
The iris is dragged in the direction of the peripheral anterior synechia.
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1. Huna R, Barak A, Melamed S. Bilateral iridocorneal endothelial syndrome presented as Cogan-Reese and Chandler's syndrome. J Glaucoma. 1996;5(1):60-2.
2. Shields MB. Progressive essential iris atrophy, Chandler's syndrome, and the iris nevus (Cogan-Reese) syndrome: a spectrum of disease. Surv Ophthalmol. 1979;24(1):3-20.
3. Wilson MC, Shields MB. A comparison of the clinical variations of the iridocorneal endothelial syndrome. Arch Ophthalmol. 1989;107(10):1465-8.
4. Langova A, Praznovska Z, Farkasova B. Progressive essential atrophy of the iris as a form of the iridocorneal endothelial (ICE) syndrome. Cesk Slov Oftalmol. 1997;53(6):371-80.
5. Alvarado JA, Murphy CG, Maglio M, et al. Pathogenesis of Chandler's syndrome, essential iris atrophy and the Cogan-Reese syndrome. I. Alterations of the corneal endothelium. Invest Ophthalmol
Vis Sci. 1986;27(6):853-72.
6. Howell DN, Damms T, Burchette JL Jr, et al. Endothelial metaplasia in the iridocorneal endothelial syndrome. Invest Ophthalmol Vis Sci. 1997;38(9):1896-901.
7. Halhal M, D'hermies F, Morel X, et al. Iridocorneal endothelial syndrome. Series of 7 cases. J Fr Ophtalmol. 2001;24(6):628-34.
8. Kidd M, Hetherington J, Magee S. Surgical results in iridocorneal endothelial syndrome. Arch Ophthalmol. 1988;106(2):199-201.
9. Buxton JN, Lash RS. Results of penetrating keratoplasty in the iridocorneal endothelial syndrome. Am J Ophthalmol. 1984;98(3):297-301.
NEW TECHNOLOGY: GDx VCC
ONE OF THE EARLIEST clinically identifiable changes occurring in glaucoma is
damage to the nerve fiber layer (NFL). Nerve fiber layer damage typically
precedes visual field loss, often by several years. Thus, a careful examination of
the NFL is essential to identify early patients who have developed glaucoma.
Focal NFL defects, particularly when they are juxtaposed against healthy NFL,
are easily detected ophthalmoscopically. However, diffuse or subtle NFL damage
is more difficult to appreciate. The need to objectively and accurately quantify the
NFL and differentiate normal patients from those with glaucoma led to the
development of the GDx Nerve Fiber Layer Analyzer.
This device utilizes scanning laser polarimetry (SLP) to measure the thickness of
the NFL for comparison against a normative database. The principles of SLP
utilize birefringence and retardation. Briefly, the NFL is birefringent due to the
parallel arrangement of microtubules within NFL axons. Birefringence changes
the polarization of the incident light into orthogonal planes. The time delay
between the return of these fast and slow axes is called retardation. Polarized
light passing through a birefringent medium (NFL) is split into two rays. Rays of
laser light that travel perpendicular to fibers passes through at a speed different
from those rays passing through in parallel. The phase shift results in retardation
and provides the basis for which to measure the thickness of the NFL.
Unfortunately, the cornea and, to a lesser extent, the lens are also birefringent
structures that essentially can contribute to signal noise that can artifactually alter
the analysis, much the same way a cataract can affect the results of a visual field.
Early iterations of SLP utilized a fixed corneal compensator that assumed a set
corneal polarization magnitude and axis. While this fixed corneal compensator
corrected for anterior segment aberration in the vast majority of patients, there
were patients whose corneal polarization magnitude and axis did not conform to
that of the general population, and their anterior segment birefringence was not
eliminated.1 This led to artifacts in the analysis with the true retrolenticular
birefringence not being accurately measured.
To address this problem, variable corneal compensation (VCC) has been
incorporated into the scanning laser polarimeter (GDx VCC). This device now
measures the corneal polarization axis and magnitude in all eyes, then sets the
device to cancel individual corneal birefringence so that the true retrolenticular
(retinal NFL) birefringence is accurately measured. The method that the GDx
VCC employs is quite simple. For the initial exam on all patients, a macular scan
is first obtained. Birefringence around the fovea is known to be uniform due to the
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absence of ganglion cells, and hence NFL in this region. A non-uniform pattern at
the fovea must be caused by the cornea, and an hourglass pattern indicates the
axis and magnitude of the corneal birefringence. When the variable compensator
is set to cancel the corneal birefringence, the hourglass disappears, indicating
successful corneal compensation.2
The goal of scanning laser polarimetry is to objectively and accurately
discriminate between normal patients and those with glaucoma. Previously
reported poor diagnostic precision of SLP with a fixed corneal compensator was
likely attributable to inflated intersubject variability resulting from ineffective
corneal birefringence compensation. New research using variable corneal
compensation has demonstrated success at differentiating normal patients from
those with glaucoma. The variable corneal birefringence compensation has
significantly narrowed the range of normals and much more accurately allows for
differentiation between those with and without glaucoma. The sensitivity of this
discrimination has increased greatly due to the removal of artifact stemming from
improperly compensated corneal polarization axis and magnitude.3-5 It appears
that the GDx VCC accurately measures the true retrolenticular birefringence and
provides a reproducible measurement of the thickness of the NFL. The VCC now
allows for accurate measurement of the NFL, which correlates well with both
structure as measured by optical coherence tomography6 and function as
measured by SITA perimetry.7 A normative database, which also represents
patients of African descent as well as other races prone to glaucoma, allows for a
statistical comparison of the NFL.
1. Weinreb RN, Bowd C, Greenfield DS, et al. Measurement of the magnitude and axis
of corneal polarization with scanning laser polarimetry. Arch Ophthalmol. 2002
Jul;120(7):901-6.
2. Zhou Q, Weinreb RN. Individualized compensation of anterior segment birefringence
during scanning laser polarimetry. Invest Ophthalmol Vis Sci. 2002 Jul;43(7):2221-
8.
3. Weinreb RN, Bowd C, Zangwill LM. Glaucoma detection using scanning laser
polarimetry with variable corneal polarization compensation. Arch Ophthalmol 2002;
120:218-24.
4. Garway-Heath DF, Greaney MJ, Caprioli J. Correction for the erroneous
compensation of anterior segment birefringence with the scanning laser polarimeter
for glaucoma diagnosis. Invest Ophthalmol Vis Sci. 2002 May;43(5):1465-74.
5. Medeiros FA, Zangwill LM, Bowd C, et al. Fourier analysis of scanning laser
polarimetry measurements with variable corneal compensation in glaucoma. Invest
Ophthalmol Vis Sci. 2003 Jun;44(6):2606-12.
6. Bagga H, Greenfield DS, Feuer W, et al. Scanning laser polarimetry with variable
corneal compensation and optical coherence tomography in normal and
glaucomatous eyes. Am J Ophthalmol. 2003 Apr;135(4):521-9.
7. Bowd C, Zangwill LM, Weinreb RN.Association between scanning laser polarimetry
measurements using variable corneal polarization compensation and visual field
sensitivity in glaucomatous eyes. Arch Ophthalmol. 2003 Jul;121(7):961-6.
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NEW TECHNOLOGY: CONFOCAL SCANNING LASER TOMOGRAPHY
WHILE CONFOCAL SCANNING LASER TOMOGRAPHY is not exactly a "new"
technology, its widespread use in clinical practice today merits special
mentioning. The Heidelberg Retinal Tomograph II (HRT II) offers a combined
approach for detection of both glaucoma and macular edema.
For glaucoma detection, the HRT II obtains a series of optical section images of
the optic disc and peripapillary retina at several depths. This series of images is
combined layer-by-layer into a three-dimensional image remarkably similar to a
CT scan. The HRT II gives both a pictorial image of the disc and cup as well as
numerical values of several disc parameters. Data obtained from a patient is
compared against a normative database in the Moorfields Regression Analysis.
The Moorfields Regression Analysis classifies eyes based upon the relationship
between the cup and rim area, among other parameters. The fact that the HRT II
linear regression analysis takes into account the overall disc area makes the
device more sensitive than clinical assessment of stereoscopic optic disc
photographs in distinguishing between healthy patients and those with early
glaucoma.1
Confidence intervals are set at 95% and 99.9%. That is, if the data obtained on a
patient shows that the area of the neuroretinal rim is larger than or equal to that
found in 95% of the patients in the normative database, the patient is classified as
"within normal limits." If the area of the neuroretinal rim for the patient falls
between 95% and 99.9% of the area for the neuroretinal rim of patients in the
normative database, the patient is classified as "borderline." If the patient's
obtained data indicates that 99.9% of the patients in the normative database have
more area to the neuroretinal rim, the patient is labeled as "outside normal limits."
These analyses are performed for several areas of the disc. Following a patient
for change over time can be done either with the stereometric parameters or by
using the Progression and Change Probability program, which is the preferred
method.
After an image is obtained, the operator must manually plot the edge of the disc
with a "contour line." This can be seen as a source of introduced error, as the
analysis is highly dependent upon the correct determination of the disc contour.
Further, the delineation between the cup and rim is accomplished through a
reference plane. The average thickness of the papillo-macular bundle located at
350º to 356º has been found to be, on average, 50µm. This is the bundle that
remains intact through disease progression. The separation of rim from cup is set
50µm below the average thickness of this area. Essentially, everything above the
reference plan is rim, and everything below is cup. This has been argued to be
another source of introduced error.
However, importing the reference plane and contour line into successive analyses
compensates for any introduced error. The Progression and Change Probability
program negates any sources of introduced error and remains a powerful feature
of the HRT II. Further, the Progression and Change Probability program can
operate without the operator ever defining a contour line. Built-in software
automatically, objectively compares subsequent patient exams against the
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original baseline exam and identifies significant changes. Measurement of disc
stereometric parameters is highly reproducible.2 There are sensitive parameters
to indicate the quality of captured images and follow-up exams that are unfocused
by more than 1.00D are easily identified. Thus, the HRT II remains an outstanding
device to measure changes in disc parameters over time.3 Further, the HRT II
can meet or exceed the disc topographic change detection performance of even
the most experienced clinicians.4 The ability to detect subtle change in the disc
topography over time is critical because this pathological alteration frequently
occurs prior to the onset of visual field progression and may be one of the first
indications of glaucomatous deterioration.5,6 The ability to detect change over
time remains the greatest strength of the HRT II.
The HRT II also provides an objective way to measure retinal edema. The
macular edema module of the HRT II analyzes signal width. It then takes into
account signal width and retinal reflectance at each retinal location obtained in the
optic slices to generate an index that is sensitive to the presence of retinal edema.
1. Wollstein G, Garway-Heath DF, Fontana L, et al. Identifying early glaucomatous
changes. Comparison between expert clinical assessment of optic disc photographs
and confocal scanning ophthalmoscopy. Ophthalmology. 2000;107(12):2272-7.
2. Miglior S, Albé E, Guareschi M, et al. Intraobserver and interobserver reproducibility
in the evaluation of optic disc stereometric parameters by Heidelberg retina
tomograph. Ophthalmology 2002; 109:1072-7.
3. Burgoyne CF, Mercante DE, Thompson HW. Change detection in regional and
volumetric disc parameters using longitudinal confocal scanning laser tomography.
Ophthalmology. 2002 Mar;109(3):455-66.
4. Ervin JC, Lemij HG, Mills RP, et al. Clinician change detection viewing longitudinal
stereophotographs compared to confocal scanning laser tomography in the LSU
Experimental Glaucoma (LEG) Study. Ophthalmology. 2002 Mar;109(3):467-81.
5. Scheuerle AF, Schmidt E, Kruse FE, et al. Diagnosis and follow-up in glaucoma
patients using the Heidelberg retina tomograph. Ophthalmologe. 2003 Jan;100(1):5-
12.
6. Chauhan BC, McCormick TA, Nicolela MT, et al. Optic disc and visual field changes in
a prospective longitudinal study of patients with glaucoma. Comparison of scanning
laser tomography with conventional perimetry and optic disc photography. Arch
Ophthalmol 2001; 119:1492-9.
NEW INSIGHT ON TREATING GLAUCOMA
WHILE GLAUCOMA HAS LONG BEEN considered a pressure- sensitive optic
neuropathy, only recently has the benefit of intraocular pressure reduction been
scientifically proven.1-5 Recently, a study has been published that may be the only
study to include an untreated study arm of patients known to have the disease.
The Early Manifest Glaucoma Trial (EMGT) was a controlled clinical trial that
evaluated the effectiveness of reducing IOP in patients with newly detected,
previously untreated, early glaucoma.6 Results from this landmark study have
shed light on managing this condition.
The EMGT randomized 255 patients, aged 50 to 80 years with early stage
glaucoma in at least one eye, into either a treated arm or an observational arm of
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the study. Patients were detected through population-based screenings at two
cities in Sweden and were included if they had a new diagnosis of early manifest
primary open-angle glaucoma (POAG), normal-tension glaucoma, or pseudo-
exfoliative glaucoma. Patients were excluded if they had advanced visual field
defects, poor acuity in either eye, mean IOP greater than 30mm Hg or any IOP
greater than 35mm Hg, or any condition that would interfere with serial
observation for progression. Thus, the patients in the study truly had early
glaucoma only.
Patients in the treated arm received standard therapy consisting of betaxolol and
argon laser trabeculoplasty. While there was not a target pressure or desired IOP
reduction, the standard treatment lowered IOP by 25%, which was maintained
throughout the study. The patients in the observational arm were followed closely
with very sensitive indicators designed to detect progression. While some
wondered whether it was ethical to not treat patients with glaucomatous damage,
the study was designed carefully so that any untreated patient who demonstrated
progression was immediately offered treatment. Thus, no patient was allowed to
lose a significant amount of visual field while undergoing observation.
The results were somewhat surprising. After fours years of follow-up, 30% of
patients in the treated arm demonstrated progression, while 49% of the untreated
patients progressed. After six years of follow-up, 45% of the patients in the
treated group had progressed, compared to 62% of the untreated patients. While
this clearly demonstrated a benefit of treatment, it was apparent that glaucoma
progressed in a large percentage of treated patients. The time that it took for
glaucoma to progress varied greatly among patients and was sometimes rather
short, even in the treated group. However, many patients remained stable
throughout the course of the study, even in the untreated group. Results of this
study showed that each mm Hg of pressure reduction conferred approximately a
10% reduction of risk for glaucoma progression. This may force doctors to
reevaluate what constitutes a "clinically significant" pressure reduction, as small
reductions in IOP may be critical.
The EMGT clearly shows that treatment for newly diagnosed early glaucoma
should be individualized and tailored to the needs of the patient. One option could
include no initial treatment, but observation with treatment commencing if
progression is seen. The decision not to treat patients in the early stage may
postpone or obviate the need for medications.
The results of this study must be viewed in context with the limitations of this
study. Virtually all patients were Caucasian. Thus, it may not be prudent to apply
the results of this study to patients of African descent, who may have an entirely
different form of the disease. Over half of the patients had normal-tension
glaucoma, which has been shown to be largely a non-progressive disease.5 Also,
there is no data on patients with very high IOP or advanced visual field loss, and
there is no long-term follow-up of patients beyond EMGT progression.
1. Lichter PR, Musch DC, Gillespie BW, et al. Interim clinical outcomes in the
Collaborative Initial Glaucoma Treatment Study (CIGTS). Comparing initial
treatment randomized to medications or surgery. Ophthalmology 2001; 108:1943-
53.
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2. Sommer AS, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and
primary open angle glaucoma among White and Black Americans. The Baltimore Eye
Survey. Arch Ophthalmol 1991;109:1090-5.
3. Kass MA, Heurer DK, Higginbotham EJ. Et al. The Ocular Hypertension Treatment
Study. A randomized trial determines that topical ocular hypotensive medication
delays or prevents the onset of primary open angle glaucoma. Arch Ophthalmol
2002;120:701-13.
4. The Advanced Glaucoma Intervention Study Investigators. The Advanced Glaucoma
Intervention Study (AGIS): 7. The relationship between control of intraocular
pressure and visual field deterioration. Am J Ophthalmol 2000; 130:429-40.
5. Collaborative Normal Tension Glaucoma Study Group. Comparison of glaucomatous
progression between untreated patients with normal tension glaucoma and patients
with therapeutically reduced intraocular pressures. Am J Ophthalmol 1998;126:487-
97.
6. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M, for the Early
Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma
progression. Arch Ophthalmol 2002;120:1268-79.
Other reports in this section
●
●
●
●
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NORMAL TENSION GLAUCOMA
Signs and Symptoms
Like most chronic forms of glaucoma, symptoms do not manifest
in normal tension glaucoma (NTG) until very late in the disease
when the patient suffers from a nearly extinguished visual field.
The patient is typically elderly, and there is a female
preponderance. It is not clear if there is a hereditary component,
thus there is a variable family history. Many patients with NTG
also possess vasospastic conditions, such as migraine and
Raynaud's phenomenon. There appears to be an increased
prevalence of known systemic autoimmune diseases in
association with NTG.1 Examination will reveal glaucomatous
atrophy of the optic disc similar to that seen in other forms of
chronic glaucoma, open anterior chamber angles, and
occasionally disc hemorrhages emanating from the superior
temporal or inferior temporal aspect of the disc in the nerve fiber Inferiorly located disc hemorrhage
in NTG.
layer. The visual field defects observed are similar to those seen
in primary open-angle glaucoma (POAG), though they tend to be deeper, steeper sided, and more
often threaten or split fixation.2,3 However IOP exceeding a statistically normal range (in most reports,
21mm Hg) cannot be documented.
Pathophysiology
The pathophysiological process underlying NTG is unclear and is, at best, speculative. For quite
some time, it was unclear if IOP played a role in the pathogenesis of NTG or whether IOP reduction
benefited patients with the condition. However, results of the Collaborative Normal Tension Glaucoma
Study (CNTGS) indicated that IOP played at least a role in the development of NTG, and IOP
reduction without causing cataracts could benefit a number of patients at risk of progression.4,5
Patients determined to be more at risk of progression included females, migraine suffers (many of
whom were female), and those manifesting a disc hemorrhage.6 Interestingly, older age, higher
average IOP, and field loss threatening fixation were not seen as risk factors for progression.6
While there has been some thought that NTG was a vascular perfusion problem, new research
seems to indicate a potential autoimmune involvement in pathogenesis. Patients with NTG may have
increased prevalence of monoclonal paraproteinemias.7 Paraprotein-emias have been seen in
patients with peripheral motor and sensory neuropathies and are considered causative agents in
several peripheral neuropathies in which antineuronal targets of these proteins have been identified.8
Kremmer and associates found greater incidence of antiphospholipid antibodies (particularly IgG
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anticardiolipin antibodies) in patients with NTG compared to those with POAG and age-matched
control patients.9
Wax and associates10 and Tezel and associates11 found that serum from patients with NTG
contained high titers of antibodies against retinal proteins, including rhodop-sin and heat shock
proteins (HSP). HSPs are a family of cellular chaperone proteins considered neuroprotective because
their expression is induced in neurons to ameliorate damage caused by various stress conditions,
such as ischemia and excitotoxicity. Heat shock proteins are significant autoantigens and have been
implicated in a number of human autoimmune diseases.
Management
Before embarking on any therapeutic management of patients suspected of having NTG, remember
that many other conditions can be confused with and misdiagnosed as NTG. These include
congenital nerve anomalies such as tilted disc and morning glory syndrome, chronic angle closure,
compressive lesions, and undiscovered POAG. The thorough examination includes gonioscopy to
eliminate angle closure as a possibility and pachymetry to identify thin corneas (which by themselves
may offer increased risk as well as the possibility that they may cause falsely lower IOP
measurements). If the disc is unusual, a second opinion may be warranted to identify possible
congenital anomalies.
Should NTG be strongly suspected, early treatment may not be prudent. Results of the CNTGS have
shown that NTG is slowly- or non-progressive in the majority of cases. Thus, those patients destined
to be slowly progressive or non-progressive derive no benefit from treatment, only risks. It is
advocated that patients with NTG be observed for a period to establish the rate of progression or
stability in each individual patient.6 Patients who manifest risk factors for progression such as
migraine and disc hemorrhage may need to be monitored more closely. When progression has been
conclusively demonstrated, IOP-lowering therapy may be initiated. However, should fixation be split
or threatened, early treatment may be employed, though the CNTGS has shown that these patients
are at no greater risk of progression. A 30% reduction in IOP from the mean baseline is advocated by
most. Medications that have been typically avoided are the beta-blockers and alpha-adrenergic
agonists, mostly due to a fear of diminishing perfusion to the optic nerve. It is interesting to note that
the CNTGS avoided these medications. Brimonidine, however, has been used recently due to a
perceived (though not clinically proven) neuroprotective effect. Prostaglandins have been recently
advocated in the management of NTG, as they have the potential to lower IOP within the statistically
normal range demonstrated in NTG. Pressure reductions of 15% to 30% have been seen in NTG in
response to prostaglandin therapy.12,13
Clinical Pearls
●
Pachymetry should be done to differentiate those patients with POAG masked by a thin cornea
from those patients with NTG.
●
Patients younger than 50 years, those with markedly asymmetric presentations, and those with
rapidly progressive disease should be considered for neuroradiologic imaging in order to rule
out the possibility of a mass lesion masquerading as NTG. However, routine imaging on every
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NTG suspect is not advocated.
●
Carefully rule out masqueraders such as tilted disc syndrome, megalopapillae, secondary
glaucomas, angle-closure glaucoma, and undiscovered POAG prior to diagnosing any patient
with NTG.
●
It has been seen that NTG is frequently slowly progressive and even non-progressive. It is
crucial to follow these patients for a period of time to establish the rate of progression in each
individual case. Those not demonstrating progression do not benefit from pressure reduction
and should be treated with close observation instead.
●
Do not rush to make a diagnosis and initiate treatment.
1. Cartwright MJ, Grajewski AL, Friedberg ML, Anderson DR, Richards DW. Immune-related disease and
normal tension glaucoma. A case-control study. Arch Ophthalmol 1992; 110:500-02.
2. Caprioli J, Spaeth GL. Comparison of visual field defects in the low-tension glaucomas with those in the
high-tension glaucomas. Am J Ophthalmol 1984:97:730-7
3. Hitchings RA, Anderton SA. A comparative study of visual field defects in low-tension glaucoma and chronic
simple glaucoma. Br J Ophthalmol 1983;67:818-21.
4. Collaborative Normal Tension Glaucoma Study Group. Comparison of glaucomatous progression between
untreated patients with normal tension glaucoma and patients with therapeutically reduced intraocular
pressures. Am J Ophthalmol. 1998;126:487-97.
5. Collaborative Normal Tension Glaucoma Study Group. The effectiveness of intraocular pressure reduction
in the treatment of normal tension glaucoma. Am J Ophthalmol 1998;126:495-505.
6. Drance S, Anderson DR, Schulzer M, for The Collaborative Normal Tension Glaucoma Study Group. Risk
factors for progression of visual field abnormalities in normal tension glaucoma. Am J Ophthalmol
2001;131:699-708.
7. Wax MB, Barrett DA, Pestronk A. Increased incidence of paraproteinemia and autoantibodies in patients
with normal pressure glaucoma. Am J Ophthalmol 1994;117:561-78.
8. Ropper AH, Gorson KC. Current concepts: neuropathies associated with paraproteinemia. N Engl J Med
1998;338:1601-7.
9. Kremmer S, Kreuzfelder E, Klein R, et al. Antiphosphatidylserine antibodies are elevated in normal tension
glaucoma. Clin Exp Immunol 2001;125:211-5.
10. Wax MB, Tezel G, Saito I, et al. Anti-Ro/SS-A positivity and heat shock protein antibodies in patients with
normal pressure glaucoma. Am J Ophthalmol 1998;125:145-57.
11. Tezel G, Seigel GM, Wax MB. Autoantibodies to small heat shock proteins in glaucoma. Invest Ophthalmol
Vis Sci 1998;39:2277-87.
12. Greve EL, Rulo AH, Drance SM, Crichton AC, Mills RP, Hoyng PF. Reduced intraocular pressure and
increased ocular perfusion pressure in normal tension glaucoma: a review of short-term studies with three
dose regimens of latanoprost treatment. Surv Ophthalmol 1997 Feb;41 Suppl 2:S89-92
13. McKibbin M, Menage MJ. The effect of once-daily latanoprost on intraocular pressure and pulsatile ocular
blood flow in normal tension glaucoma. Eye 1999;13(Pt 1):31-4.
Other reports in this section
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PRIMARY CHRONIC ANGLE CLOSURE GLAUCOMA
Signs and Symptoms
The patient with primary chronic angle-closure glaucoma (CACG) typically is older and
asymptomatic.1 Women are more commonly affected than men. Hyperopia is commonly
encountered. Patients of Asian descent are the most predisposed to CACG, with Eskimos being the
most represented group with CACG. Caucasian patients are affected to a lesser extent, and patients
of African descent are affected even less.
Biomicroscopically, there will be a shallow anterior chamber and narrow angles by Von Herrick
estimation method. However, the chamber depth is typically deeper in CACG than primary acute
angle-closure glaucoma. There will be characteristic glaucomatous damage to the optic disc and
visual field. The distinguishing characteristic is the absence of visible anterior chamber angle
structures upon the performance of gonioscopy. The angle may be appositionally closed and opened
upon manual pressure on the 4-miror goniolens, or the angle may be synechially closed with broad
areas of peripheral anterior synechia (PAS). The superior and temporal quadrants of the anterior
angle may be the earliest sites of the synechial angle closure, with gradual extension to the nasal
quadrant, until the angle closes at the inferior quadrant.2 Other features of CACG include a smaller
corneal diameter, shorter axial length, shallower anterior chamber, thicker lens, more relative anterior
location of the lens, swelling of the ciliary process and anterior rotation of the ciliary body.3
Pathophysiology
Anatomical features act in concert to cause shallowing of the anterior chamber. As a patient ages,
thickening of the crystalline lens leads to a relative pupil block that exacerbates the condition. This all
acts to put the iris into apposition with the trabecular meshwork or cornea. In the absence of
secondary causes, this is considered to be a primary angle closure. Due to the fact that the closure is
slow, there is an absence of symptoms that would typify an acute angle closure. Thus, patients are
unaware of the process. Chronic angle closure denotes an angle with areas that are closed
permanently with PAS. In angles that have closure without the formation of PAS, the term chronic
appositional closure is often used. However, appositional closure often will lead to PAS if untreated.
In chronic angle closure, the intraocular pressure (IOP) may be initially low and elevates
asymptomatically as more of the angle becomes compromised. Peripheral anterior synechia may
occur after acute or subacute attacks of angle closure.
While in most cases, there is asymmetric closure involving first the superior angle, there can also be
an even circumferential closure that slowly progresses symmetrically. This has been termed "creeping
angle closure" and appears as an angle that becomes progressively more shallow over time.4
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Management
All cases of primary angle closure need to undergo laser peripheral iridotomy (LPI) as soon as
possible after diagnosis. This allows a communication for aqueous to flow from the posterior chamber
to the anterior chamber bypassing any pupil block that may be present. This can allow for the
backward relaxation of the iris and a deepening of the chamber and opening of the angle. This is a
safe method to open the angle following chronic closure.5 However, while LPI can alter the anatomic
status of the angle, there often will be elevated IOP despite a laser-induced open anterior chamber
angle. This is most likely due to damage to the trabecular meshwork from appositional and synechial
closure. In CACG eyes, the trabecular architecture has lost its regular arrangement, with fewer and
narrower trabecular spaces and fusion of the trabecular beams in areas. In addition, there is evidence
of loss of endothelial cells and reactive repair processes.6 Despite the presence of a patent LPI, most
eyes with CACG presenting with elevated IOP and having both optic disc and visual field damage in
both populations required further treatment to control IOP, including trabeculectomy and medical
therapy.7 Medical therapy that has been seen to be successful in ameliorating the IOP in eyes with
CACG include beta blockers, miotics, alpha-2 adrenergic agonists, and prostaglandins.8,9 Argon laser
iridoplasty has been seen as another option for the management of CACG as it can affect the shape
of the peripheral iris and prevent this condition from deteriorating.10
Clinical Pearls
●
After the anterior chamber angle has been successfully opened by LPI, the IOP may still be
elevated. Many will erroneously think that the patient has now developed primary open-angle
glaucoma. In actuality, the trabecular meshwork has been damaged by the appositional
closure. This situation is like the trabecular dysfunction seen in angle-recession glaucoma.
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Gonioscopy must be done on all open angle glaucoma patients at least annually to ascertain
that the patient is not developing a concurrent angle-closure mechanism.
1. Bonomi L, Marchini G, Marraffa M, et al. Epidemiology of angle-closure glaucoma: prevalence, clinical
types, and association with peripheral anterior chamber depth in the Egna-Neumarket Glaucoma Study.
Ophthalmology. 2000;107(5):998-1003.
2. MOK KH, Lee VW. Synechial angle closure pattern in Chinese chronic primary angle-closure glaucoma
patients. J Glaucoma. 2001;10(5):427-8.
3. Wang T, Liu L, Li Z, et al. Studies of mechanism of primary angle closure glaucoma using ultrasound
biomicroscope. Zhonghua Yan Ke Za Zhi. 1998;34(5):365-8.
4. Lowe RF. Primary creeping angle closure glaucoma. Br J Ophthalmol 1964;48:544.
5. Hsiao CH, Hsu CT, Shen SC, et al. Mid-term follow-up of Nd:YAG laser iridotomy in Asian eyes. Ophthalmic
Surg Lasers Imaging. 2003;34(4):291-8.
6. Sihota R, Lakshmaiah NC, Walia KB, et al. The trabecular meshwork in acute and chronic angle closure
glaucoma. Indian J Ophthalmol. 2001;49(4):255-9.
7. Rosman M, Aung T, Ang LP, et al. Chronic angle-closure with glaucomatous damage: long-term clinical
course in a North American population and comparison with an Asian population. Ophthalmology. 2002;109
(12):2227-31.
8. Ruangvaravate N, Kitnarong N, Metheetrairut A, et al. Efficacy of brimonidine 0.2 per cent as adjunctive
therapy to beta-blockers: a comparative study between POAG and CACG in Asian eyes. J Med Assoc Thai.
2002;85(8):894-900.
9. Aung T, Wong HT, Yip CC, et al. Comparison of the intraocular pressure-lowering effect of latanoprost and
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Handbook of Ocular Disease Management
timolol in patients with chronic angle closure glaucoma: a preliminary study. Ophthalmology. 2000;107
(6):1178-83.
10. Zou J, Zhang F, Zhang L, et al. A clinical study on laser peripheral iridoplasty for primary angle-closure
glaucoma with positive provocative tests after iridectomy. Chung Hua Yen Ko Tsa Chih. 2002;38(12):708-
11.
Other reports in this section
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Neovascular Glaucoma
Neovascular Glaucoma
Signs and Symptoms
Patients with neovascular glaucoma (NVG) may be asymptomatic, but more typically present with a
chronically red, painful eye which often has significant vision loss. Further, there will be significant concurrent
vascular disease such as diabetes, hypertension, carotid artery disease, or giant cell arteritis (GCA). There
frequently is an antecedent history of a retinal vessel occlusion or chronic uveitis.
There will be visible neovascularization of the iris (NVI) and angle (NVA). Only rarely will NVA develop
without NVI. The patient typically has significant corneal edema and elevated intraocular pressure, often
exceeding 50-mm-Hg. There may be a shallow anterior chamber. Gonioscopically, there will be total or near-
total angle closure. Funduscopically, there typically will be evidence of retinal vessel occlusion (either artery or
vein), ocular ischemic syndrome or diabetic retinopathy.
Pathophysiology
Ischemia to ocular tissues is theorized to be the genesis of NVG. The most common causes of NVG include
ischemic central retinal vein occlusion (CRVO), diabetic retinopathy, and carotid artery disease and ocular
ischemic syndrome (OIS). Less common causes of NVG include hemi- and branch retinal vein occlusion,
retinal artery occlusion, and GCA. In terms of retinal vein occlusions, NVG typically develops within three
months of the occlusion. In terms of retinal artery occlusions, NVG typically develops within four weeks of the
occlusion.
In ischemic retinal disease, hypoxia induces vascular endothelial growth factor (VEGF), a vasoproliferative
substance, with acts upon healthy endothelial cells of viable capillaries to stimulate the formation of a fragile
new plexus of vessels (neovascularization). In cases of extreme retinal hypoxia, there are essentially very few
viable retinal capillaries available. In that instance, VEGF is theorized to diffuse forward to the nearest area of
viable capillaries, namely the posterior iris. Neovascularization buds off of the capillaries of the posterior iris,
grows along the posterior iris, through the pupil, along the anterior surface of the iris, and then into the angle.
Once in the angle, the neovascularization, along with its attendant fibrovascular support membrane, acts to both
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Neovascular Glaucoma
physically block the angle as well as bridge the angle and physically pull the iris and cornea into apposition,
thus blocking the trabecular meshwork. Peripheral anterior synechiae with permanent angle closure happens
quickly. The result is a secondary angle closure without pupil block. Due to the extremely elevated intraocular
pressure, there will be a modest amount of inflammation.
Management
If there is any degree of inflammation and ocular pain, prescribe a topical cycloplegic such as atropine 1% b.i.
d. as well as a topical steroid such as Pred Forte, Vexol, or Flarex q.i.d. Aqueous suppressants may be used in
order to temporarily reduce IOP. However, chronic medical therapy is not indicated for neovascular glaucoma.
Aqueous suppressants will temporize IOP and lead to a false sense of security as the neovascular process will
continue with further angle closure.
Ultimate management of NVG involves eradication of the vessels. This is best accomplished with pan-retinal
photocoagulation to destroy ischemic retina, minimize oxygen demand of the eye, and reduce the amount of
VEGF being released. PRP tends to be effective in causing regression and involution of anterior segment
neovascularization. If a significant amount of the angle is in permanent synechial closure, filtering surgery
must then be employed.
Clinical Pearls
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PRP has a 90 percent success rate in NVG due to diabetes if less than 270º of the angle is closed.
However, if NVG is due to ocular ischemic syndrome, PRP is less successful and 90 percent of these
patients will have count fingers vision within one year.
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In cases of NVG in elderly patients, always consider GCA as a potential etiology.
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Retinal artery occlusions develop NVG in only 17 percent of cases and typically within four weeks post-
occlusion.
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Miotics are absolutely contraindicated in any case where there is active inflammation. Prostaglandin
analogs should likewise be avoided.
Other reports in this section
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Neovascular Glaucoma
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Pars Planitis
Pars Planitis
Signs and Symptoms
The patient with par planitis is typically a younger patient
with no significant medical history. Patients are frequently
asymptomatic, but may present with modestly diminished
vision that is slowly progressive, as well as complaints of
floaters. A history of similar occurrences of symptoms may
be disclosed.
The first observable sign of pars planitis is the presence of vitreal cells in an active vitritis. The vitritis may
cause vitreous degeneration with a resultant posterior vitreous detachment. The vitritis frequently will result in
an accumulation of inflammatory exudate. The accumulation may be small (snowballs) or extensive
(snowbanks) and may occur anywhere in the fundus but is typically regulated to the inferior fundus by gravity.
There also may be the presence of cataracts, especially posterior subcapsular, and cystoid macular edema. In
extreme cases, there may be retinal neovascularization.
Pathophysiology
Pars planitis is a true posterior/intermediate uveitis that chronically affects younger, healthy patients. Pars
planitis is idiopathic and unassociated with systemic disease. However, there have been some implications of
an association of autoimmune disease (juvenile rheumatoid arthritis) and demyelinating disease. There are
exacerbations and remissions and typically this disorder runs a very long course. Inflammatory mediators will
increase vasopermeability of retinal capillaries resulting in posterior segment inflammatory cells as well as
cystoid macular edema (CME). Vision loss occurs due to cataracts and CME.
Management
Pars planitis is generally benign. Vision loss tends to be mild, if it occurs at all. Only in extreme cases is vision
loss profound. In these cases, the cause of vision loss is retinal neovascularization with its attendant
complications of vitreous hemorrhage and tractional retinal detachment. As pars planitis is typically a relatively
benign disease, treatment should be conservative and often involves only periodic monitoring.
If treatment is undertaken due to mild vision loss from cystoid macular edema or vitreous clouding, then
steroids form the cornerstone. Topical steroids are employed only if there is a concomitant anterior uveitis.
However, in these cases, the anterior chamber reaction is not a true anterior uveitis, but a spill-over from the
posterior uveitis. Thus, topical steroids are rarely indicated. Oral prednisone is more commonly used. However,
once a commitment to use oral steroids is made, typically they must be used for months. With this treatment
comes the possible attendant complications of steroid induced cataracts and glaucoma. In severe cases, sub-
tenon’s injections of steroids may be used, as well as vitrectomy to clear the vitreous and cyclocryotherapy to
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destroy the inflamed areas and infiltrates. Topical and oral non-steroidal anti-inflammatory agents have been
used to treat attendant CME with some success.
In most cases, pars planitis is unassociated with systemic disease. However, in order to avoid a possible mis-
diagnosis, have the patient tested for both syphilis and sarcoidosis as these diseases may present a similar
clinical picture.
Clinical Pearls
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Posterior vitreous detachment is rare in younger patients; however, PVD is quite common in pars
planitis. Consider pars planitis when encountering PVD in younger patients.
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Always consider pars planitis in cases of asymptomatic vitreous cells in healthy, younger patients.
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When suspecting pars planitis, carefully examine the inferior retina and vitreous for snowballs and
snowbanking.
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Pars planitis can be safely monitored without treatment. If the decision to treat is made, however,
expect to treat with oral steroids for several months.
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If pars planitis is definitively diagnosed, medical testing is unnecessary. However, if the diagnosis is in
question, remember that the differential includes sarcoidosis, syphilis, multiple sclerosis with vascular
sheathing and intermediate uveitis, toxoplasmosis, and toxocariasis.
Other reports in this section
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Choroidal Rupture
Choroidal Rupture
Signs and Symptoms
Patients who experience choroidal rupture are often
younger and involved in activities, such as ball sports,
which expose them to potential high-rate impact trauma to
the eye or adenexa. Patients have a history, either recent
or antecedent, of direct or contrecoup injury to the eye and
surrounding structures.
Choroidal ruptures may be single or multiple and may
affect any part of the posterior segment. In recent trauma,
there may be hemorrhage in any layer ranging from the
choroid to the vitreous. However, if the trauma was many
years antecedent, there will be no hemorrhage unless
choroidal neovascularization has developed. Visual acuity
and visual field may be dramatically reduced or may be
normal and the patient is asymptomatic.
Ophthalmoscopically, you will note a linear disruption
that may be crescent-shaped. Often, the rupture will have
the concave aspect toward the disc. There is usually
significant reactive RPE hyperplasia, giving the rupture a
pigmented appearance.
Pathophysiology
Direct or contrecoup injury can precipitate a choroidal rupture. Hemorrhage and edema may be present
initially, but will resolve. Typically, reactive hyperplasia gives the rupture a heavily pigmented appearance.
Often, the overlying retina is undisturbed in choroidal rupture. However, if the RPE is disturbed and becomes
hyperplastic and invades the sensory retina, visual dysfunction ensues.
Due to the subsequent disruption of Bruch’s membrane that occurs in choroidal rupture, choroidal neovascular
membranes may develop within the rupture. This may be a late development that can occur up to five years
after the precipitating trauma.
Management
There is no direct intervention in the acute phase of choroidal rupture. Educate patients about their condition
and prescribe protective eye wear. Monitor the patient funduscopically for at least five years for the
development of choroidal neovascularization within the rupture scar. Any late bleeding should receive a
fluorescein angiogram to determine if a choroidal neovascular membrane has developed. Choroidal
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Choroidal Rupture
neovascular membranes resulting from choroidal rupture have a tendency to spontaneously involute. For this
reason, laser photocoagulation is indicated only if there is imminent threat to vision.
Clinical Pearls
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Choroidal neovascularization can occur five years after the initial trauma.
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Sub-retinal hemorrhage from choroidal neovascularization is the most common cause of late vision loss.
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As the retina overlying a choroidal rupture may be unaffected, patients may retain excellent visual
function and present asymptomatically years after the trauma. A patient may have a rupture between the
disc and macula, yet retain normal acuity.
Other reports in this section
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Axenfeld-Rieger Syndrome
Axenfeld-Rieger Syndrome
Signs and Symptoms
Patients displaying Axenfeld-Rieger (A-R) syndrome are
generally asymptomatic. The condition is diagnosed based
upon findings from routine biomicroscopic and
gonioscopic evaluation. Historically, this condition was
incorporated under the broader heading of anterior chamber
cleavage syndromes, and included Axenfeld’s anomaly,
Axenfeld’s syndrome, Rieger’s anomaly, and Rieger’s
syndrome. Current theory now holds that these conditions
are probably a continuum of a single developmental
disorder, hence the name Axenfeld-Rieger syndrome.
This anterior segment disorder always presents with
posterior embryotoxon (a prominent, anteriorly displaced
Schwalbe’s line) and one or more of the following findings:
iris strands adherent to Schwalbe’s line, iris hypoplasia,
focal iris atrophy with hole formation, corectopia, and
ectropion uveae. Glaucoma may develop in approximately
50 percent of patients with A-R syndrome, but is more
common in those with central iris changes and pronounced
anterior iris insertion. Non-ocular manifestations of A-R
syndrome may include developmental defects of the teeth
and facial bones, pituitary anomalies, cardiac disease,
oculocutaneous albinism, and redundant periumbilical skin.
A-R syndrome is always bilateral but may be markedly
asymmetric. The condition appears to be hereditary,
displaying an autosomal dominant inheritance pattern with variable expression.
Pathogenesis
There has been much speculation as to the embryonic pathogenesis of A-R syndrome. The current and most
widely held theory suggests a developmental arrest of specific anterior segment tissues derived from neural
crest cells, which apparently occurs late in gestation. It is not understood why such a developmental arrest
occurs, but the result is the retention of a primordial endothelial cell layer on portions of the iris and angle
structures. Contraction of these endothelial "membranes" leads to the associated abnormalities in form and
function of the anterior segment structures. Presumably, this same developmental arrest can affect other organ
systems, resulting in orofacial and other anomalies sometimes encountered in A-R syndrome.
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Axenfeld-Rieger Syndrome
Management
A-R syndrome, a congenital disorder, generally requires little therapeutic intervention. In those instances where
iris atrophy results in pseudopolycoria, patients may be fitted with opaque, cosmetic contact lenses to improve
their appearance and decrease optical aberrations.
The greatest concern in patients with A-R syndrome is the development of secondary glaucoma. In most cases,
those who develop glaucoma do so in childhood or early adulthood. Still, patients must be monitored
throughout life for elevations in intraocular pressure and optic nerve head changes. Glaucoma therapy for
patients with A-R syndrome follows the same therapeutic algorithm as for primary open angle glaucoma,
however miotics are reported to be less effective in this condition. Typical therapy begins with topical -
blockers (e.g., Betoptic-S) or topical carbonic anhydrase inhibitors (e.g., Azopt). Unfortunately, many of these
glaucoma cases become recalcitrant, and surgical intervention is often necessary.
Clinical Pearls
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Axenfeld-Rieger syndrome is described as a rare, congenital ocular disorder. Still, these authors have
encountered many patients with manifestations of A-R syndrome, some of which are exceedingly
subtle. In general, A-R syndrome is more academically interesting than it is clinically challenging.
Glaucoma must be a concern in every patient presenting with this disorder. In fact, when glaucoma
does occur, it can be quite severe. In addition, patients with A-R syndrome should undergo both a
comprehensive medical and dental evaluation to rule out non-ocular manifestations.
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Because of the known inheritance pattern and variable expression, recommend ocular evaluation for all
family members when you detect A-R syndrome.
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