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).

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.

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 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.")

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.

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

• 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.

ANTERIOR UVEITIS
 SIGNS AND SYMPTOMS
The typical presentation of anterior uveitis involves pain,
photophobia and excessive tearing. Patients report a deep, dull
aching of the involved eye and surrounding orbit. Associated
sensitivity to lights may be severe; often, these patients will present
wearing dark sunglasses. The excessive tearing occurs secondary to
increased neural stimulation of the lacrimal gland, and is not
associated with a foreign body sensation.

Visual acuity is not usually impaired to any great extent (20/40 or better is common), although patients may
report some haziness. Accommodative tasks, however, may prove more difficult and uncomfortable.
Inspection may reveal mild to moderate congestion of the lids, resulting in pseudoptosis. You'll typically
see a deep perilimbal injection of the conjunctiva and episclera, although the palpebral conjunctiva is
characteristically normal. The cornea may display mild edema upon biomicroscopy. In more severe
reactions, you may observe grayish brown endothelial deposits, known as keratic precipitates.

The hallmark signs of anterior uveitis are "cells and flare." Cells are leukocytes (white blood cells) floating
in the convection currents of the aqueous; flare refers to liberated protein from the inflamed iris or ciliary
body which gives the aqueous a particulate, or smoky, appearance. The iris may adhere to the lens capsule
(posterior synechia) or, less commonly, to the peripheral cornea (anterior synechia). Additionally, you may
see granulomatous nodules within the iris stroma.

Intraocular pressure in the affected eye is initially reduced 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. Inflammation may be associated with underlying systemic disease, or it may occur as a direct result
of ocular trauma. Occasionally, inflammatory reactions in adjacent tissues (e.g., keratitis), can induce a
secondary uveitis.

Uveitis can be either acute or chronic. The chronic form is more often associated with systemic disorders
including, but not limited to, ankylosing spondylitis, Behçet's syndrome, inflammatory bowel disease,
juvenile rheumatoid arthritis, Reiter's syndrome, sarcoidosis, syphilis, tuberculosis, and Lyme disease.
Chronic uveitis most likely occurs due to an immunopathological mechanism which is not fully understood.

MANAGEMENT
There are two primary goals when managing anterior uveitis. First, immobilize the iris and ciliary body to
decrease pain and prevent exacerbation of the condition. Second, quell the inflammatory response. Begin
by cyclopleging the patient with homatropine 5% TID/QID, scopolamine 0.25% BID/QID or atropine 1%
BID, depending upon the severity of the reaction. Next, prescribe a topical steroid Q2-3H, or more often if
the reaction is severe. If there's a posterior synechia present, attempt to break the adhesion in the office
using atropine 1% and phenylephrine 10%. Treat secondary elevations in IOP using standard anti-glaucoma
agents, such as timolol 0.5% BID or dorzolamide 2% TID.

Avoid pilocarpine in uveitic glaucoma, as it will only serve to worsen the inflammatory response by
mobilizing the uveal tissues. After beginning treatment, re-evaluate the patient every one to seven days
depending on the severity of the reaction. As the uveitis resolves, discontinue the cycloplegics and taper the
steroids to QID or TID. Generally, it is better to taper slowly rather than abruptly, and patients may need to
remain on steroid drops daily or every other day for several weeks. In recalcitrant uveitis which is
unresponsive to conventional therapy, consider injectible steroids such as methylprednisolone 60mg or
even oral steroids such as prednisone 60 to 80mg.
CLINICAL PEARLS

• Acute anterior uveitis results most commonly as a result of blunt ocular trauma. In most instances,
these cases resolve without incident and do not recur when properly managed.
• Consider any cases of recurrent uveitis, defined as three or more unexplained incidents, to be
representative of underlying systemic inflammatory disease until proven otherwise. Hematologic
testing is indicated for any 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 also important in identifying both sarcoidosis and
tuberculosis. A Lyme titer is also recommended if you suspect that the patient may have been
bitten by a deer tick.
• Always perform a comprehensive, dilated fundus evaluation in these cases. Anterior uveitis may
actually constitute a "spillover" of posterior ocular inflammation.

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.

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.

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.

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.

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 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

• 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.
• In cases of NVG in elderly patients, always consider GCA as a potential etiology.
• Retinal artery occlusions develop NVG in only 17 percent of cases and typically within four
weeks post-occlusion.
• Miotics are absolutely contraindicated in any case
where there is active inflammation. Prostaglandin
analogs should likewise be avoided.

BACTERIAL KERATITIS
Signs and Symptoms

Culture-proven Pseudomonas keratitis with

The patient with bacterial keratitis will generally mucopurulent discharge.
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. Often, there will be a history of
contact lens wear, which is the most common

Hypopyon in bacterial keratitis.

precipitating condition. Corneal trauma or pre-existing keratopathy are also common precipitating
conditions.1

Mucopurulent discharge may emanate from the lesion. The cornea may be 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 bacterial keratitis, injection is typically 360 degrees
rather than sectoral as seen in non-infectious keratitis. A pronounced anterior chamber reaction,
often with hypopyon, is present in severe cases. Intraocular pressure may be reduced due to
secretory hypotony of the ciliary body, but may 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, the cornea is prone to colonization and infection by
pathogenic bacteria. Factors known to compromise corneal defenses include direct corneal
trauma, chronic eyelid disease, systemic immune disease, tear film abnormalities affecting the
ocular surface and hypoxic trauma from contact lens wear.2

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 by releasing
numerous enzymes that directly affect and damage stromal tissue.

The collagen of the corneal stroma is poorly tolerant of the bacterial and leukocytic enzymes, and
undergoes degradation, necrosis and thinning. This leads to scarring of the cornea. As thinning
advances, 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 Pseudo-monas aeruginosa.
Throughout North America, the most common infective organism in bacterial keratitis is
Staphylococcus aureus, and it appears that there is an increased incidence of Gram-positive
recovery in infectious keratitis.3

Management

Proper diagnosis and prompt therapy are essential to preserve vision in bacterial keratitis. The
first step in management should be to obtain corneal scrapings for microbiologic studies. The
standard of care describes the use of a platinum spatula with plating directly onto blood and
chocolate agar medium. However, the effectiveness of the fluoroquinolones has led many
practitioners away from this standard. Identification, as well as sensitivity studies, will aid in
management. An alternative for treatment of less severe keratitis is a mini-tip calcium alginate
culturette and transport-media-containing carrier. The results of this technique compared to
platinum spatula collection and plating was 83.3% sensitivity and 100% specificity. The
conservative approach supports culturing most, if not all, suspected infectious ulcers. We
advocate obtaining cultures for central lesions that threaten vision, are at risk of perforation, and
in institutionalized patients in nursing homes and hospitals where methicillin-resistant Staph.
aureus infections are possible.4

If the patient has been cultured, initiate broad-spectrum, empirical antibiotic therapy prior to
receiving the results. Monotherapy with fluoroquinolone eye drops has been shown to result in
shorter duration of intensive therapy and shorter hospital stay when compared with combined
fortified therapy (tobramycin-cefazolin). This finding may have resulted from quicker clinical
response of healing as a result of less toxicity found in the patients treated with fluoroquinolones.
However, as some serious complications were encountered more commonly in the
fluoroquinolone group, caution should be exercised in using fluoroquinolones in large, deep
ulcers in the elderly.5

Despite clear efficacy of fluoroquinolones in the management of bacterial keratitis,2,6-8

consideration must be given to the increasing resistance to these drugs. Since their inception,
there has been a rise in the incidence of bacterial isolates in keratitis that exhibit resistance to the
early generation fluoroquinolones.2,3,9 One method of combating the increasing problem of
fluoroquinolone resistance and rising level of Gram-positive infections is to use the new fourth-
generation topical fluoroquinolones.

Traditional initial monotherapy has utilized 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 second-generation fluoroquinolone,
Ocuflox (ofloxacin, Allergan), is also an effective treatment for bacterial keratitis.7 Both
fluoroquinolones have been proven to be as effective for managing bacterial keratitis as the
previously used fortified antibiotics, but with significantly fewer side effects. Unfortunately,
bacterial resistance to the second-generation fluoroquinolones has been increasing, especially
among the Gram-positive organisms. The two most recently available fourth-generation
fluoroquinolones, moxifloxacin (Vigamox, Alcon) and gatifloxacin (Zymar, Allergan), have a
greatly lowered resistance rate while providing much greater Gram-positive activity than previous
generation fluoroquinolones.10 In the future, Zymar or Vigamox dosed on an hourly basis may
become the mainstay therapy for bacterial keratitis.

Strong cycloplegia is also mandatory in order to increase patient comfort and minimize
inflammation. The weakest cycloplegic that should be employed is scopolamine 0.25% tid. If this
is insufficient, then atropine 1% bid is indicated. Adjunctive use of cold compresses will also help
to reduce inflammation.

The patient should be followed daily until the infection is well controlled. If the results of cultures
and sensitivities show that the initially prescribed antibiotic is appropriate for the infective
organism, or if the patient shows signs of clinical improvement (the ulcer does not worsen, and
pain and photophobia are reduced) at the 24 to 48 hour follow-up visit, a topical corticosteroid
such as prednisolone acetate 1% or loteprednol etabonate 0.5% q2h can be added to speed
resolution and decrease corneal scarring.

While steroids have historically been avoided in the management of infectious keratitis, judicious
use can be beneficial. Antibiotics can suppress the infective organism, while corticosteroids can
inhibit the corneotoxic inflammatory response. It has been feared that the immunosuppressive
effects of steroids could enhance bacterial replication and worsen infection. However, if the
chosen antibiotic is effective against the organism, then the concurrent use of steroids will not
inhibit the bactericidal effect of the antibiotic.1117 But note that steroids should not be employed
until the antibiotic has been given enough time to sterilize the ulcer, minimally 24 hours. One also
must be certain that there is not a simplex viral, fungal, or protozoan infection prior to the initiation
of topical steroids. Also, steroids should only be used in conjunction with true bactericidal
antibiotics such as fluoroquinolones.

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 bactericidal 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 to 48 hours after you initiate antibiotic therapy. If you wait until the ulcer
re-epithelializes before adding a steroid, the beneficial effects will be reduced. A
cautionary note: Be comfortable that the antibiotic has sterilized the ulcer before
instituting the steroid.

PANNUS

Definition: The word "pannus" takes its origin from the Latin
meaning "a piece
of cloth." Relating to the eye, it is pathologically defined as a
superficial vascularization of the cornea with infiltration of
inflammatory-connective-granulation tissue. Pannus is not a
diagnosis; it is a finding that results secondary to another
disease process.111
Pannus lesion.
Diseases associated with pannus

• LASIK2
• Allergic conjunctivitis3,11
• Toxic conjunctivitis3
• Neonatal conjunctivitis3
• Chlamydial conjunctivitis3,11
• Fuch's endothelial dystrophy4,5
• Congenital hereditary endothelial dystrophy6
• Superior limbic keratoconjunctivitis of Theodore7
• Terriens marginal degeneration7
• Mycobacterial tuberculos pannus8
• Leprosy8
• Aniridia9
• Keratoconjunctivitis10

Immune Stromal (Interstitial) Keratitis

Signs and Symptoms

Patients with active immune stromal keratitis (ISK) will

present with pain, photophobia, lacrimation, and
blepharospasm. Vision is typically reduced in the
acute, active phase. The presentation may be either
unilateral or bilateral. There will often be a history of
ocular infection or systemic disease. However, ISK
may be the initial manifestation of an unknown

Active herpes simplex stromal keratitis.

underlying systemic disease. Occasionally, ISK is idiopathic. ISK runs a chronic, indolent course
and may persist for many months.

There will be a single or multiple white patches of infiltration and inflammation within the corneal
stroma. There will be concurrent stromal edema as well as stromal vascularization. Typically, the
overlying epithelium is intact. If there is epithelial disruption, it will be much smaller in area than
the underlying inflammation. Corneal thinning may result as sequelae of the chronic inflammation;
however, thinning is not a distinctive feature. There will be a secondary anterior uveitis.
Endothelial folds and keratic precipitates are common.

Pathophysiology

ISK is an immune-mediated nonsuppurative stromal inflammation with an intact epithelium. ISK is

typically associated with an often readily identifiable causative agent. Conditions causing SK
include Epstein Barr virus, herpes zoster and simplex, mumps, measles, Lyme disease,
Acanthamoeba infection, tuberculosis, syphilis, sarcoidosis and onchocerciasis. However, the
most common cause of active ISK is the herpes simplex virus, accounting for over 70% of
unilateral active cases.1 Sixty percent of cases of bilateral, active ISK are idiopathic in nature.
Syphilis is the cause of approximately 50% of bilateral inactive cases. Although syphilis is the
leading cause of inactive, bilateral ISK, it is actually responsible for less than 20% of total cases.1

It must be emphasized that there is no active microbial infection within the corneal stroma in ISK.
Rather, microbial antigens initiate a T-lymphocytic destruction of the stroma.2 Subsequent stromal
vascularization and cicatrization invariably results if the underlying cause is left untreated. The
stromal vascularization will begin during the acute phase and progress throughout the disease's
course. However, the presence of stromal vascularization is not required in order to make this
diagnosis (as was previously thought).

There are two types of ISK that may occur during herpes simplex infections: necrotizing and non-
necrotizing. Necrotizing herpetic ISK is a more severe form of herpetic stromal keratitis and
manifests as a dense, cheesy, yellow-white stromal infiltration often following recurrent herpetic
disease. There will be epithelial ulceration, stromal edema, dense vascularization, profound
corneal thinning, and possible perforation. Non-necrotizing herpetic ISK does not have the same
propensity to move toward ulceration, thinning, and perforation. Untreated, non-necrotizing ISK
runs an indolent, self-limiting course over several months. Fortunately, the majority of herpetic
ISK cases are non-necrotizing.

Management

Immune stromal keratitis is a self-limiting condition, which will spontaneously resolve within
several months. However, the result invariably will be profound stromal vascularization and
scarring with subsequent visual reduction. Hence, treatment is indicated. It must be remembered
that ISK is an immune stromal keratitis and not an active infectious process. Application of a
strong steroid such as prednisolone acetate 1% q1h to q2h is optimal. Depending upon the
etiology, the patient may need to use low doses of topical steroids indefinitely. Cycloplegia and
topical lubrication will ease the patient's discomfort.

When ISK is caused by the herpes virus, therapy deviates somewhat from the above-mentioned
regimen. Lower doses of topical steroids may be employed to control the patients' disease and
symptoms. When topical steroids are used to treat herpetic immune stromal disease, prophylactic
topical antiviral medications (trifluridine) should be used concurrently.3,4 There has been no
proven benefit for the adjunctive use of oral acyclovir in the acute management of patients with
herpes simplex stromal keratitis being treated with topical corticosteroids and trifluridine.5
Herpes simplex ISK is a highly recurrent disease, with the risk related to the number of previous
recurrences.6 Long-term suppressive oral therapy with acyclovir 400mg po bid has been shown to
significantly reduce the recurrence rate of not only epithelial keratitis from herpes simplex, but
also stromal disease.7,8 Strong consideration should be given for long-term suppressive therapy
beyond one year in herpes simplex stromal keratitis.

As ISK can result from a variety of causes, a diagnostic evaluation should be initiated. Unless the
cause is obviously herpetic, medical evaluation for IK should include FTA-ABS or MHA-TP for
syphilis, PPD and chest X-ray for tuberculosis, Lyme titer for Lyme disease, and rheumatoid
factor and antinuclear antibodies for collagen vascular disease. Should a cause be elicited, the
patient should receive medical treatment directed toward the underlying cause while he or she
undergoes topical treatment.

Particular attention must be paid to patients presenting with ISK and hearing loss, signaling
Cogan's syndrome. Cogan's syndrome is an idiopathic inflammatory disease, which may present
as ISK, inflammation of other ocular structures, Meniere's-like attacks, audiovestibular
dysfunction or systemic vasculitis. Although the ocular manifestations respond to topical steroids
and are rarely serious, permanent deafness may result if systemic steroid therapy is not promptly
instituted for audiovestibular dysfunction, while major morbidity and even death may occur if
systemic sequelae such as vasculitis and aortic insufficiency are not recognized.9

Clinical Pearls

• If a patient develops ISK on the same side as a prior episode of either HSV or HZV and
there is no indication of other disease in the patient's history, then no further diagnostic
evaluation is necessary. In this case, it can safely be assumed that the cause of the ISK
is herpetic.
• Historically, ISK has been associated with syphilis as the main causative agent. Today,
however, syphilis is the main cause only in cases of bilateral, inactive ISK. By far, the
main identifiable cause of active cases of ISK is herpes simplex virus.
• In cases of active herpetic ISK, topical and oral antiviral medications have been
exceedingly disappointing therapeutically. The only use for either oral or topical antiviral
medications in herpetic IK is prophylactically to prevent epithelial ulceration when topical
corticosteroids are used and to suppress future recurrences.
• Stromal inflammatory infiltration in herpetic ISK can be difficult to differentiate from both
bacterial and fungal keratitis. However, IK will have a more intact epithelium whereas the
other entities will have ulceration. Further, IK runs an indolent course, whereas infectious
keratitis is much more aggressive.
• As in other herpetic manifestations, corneal sensitivity is reduced on the affected side.
• Suspect Cogan's syndrome in patients presenting with ocular inflammation who develop
hearing loss, vertigo, ataxia, tinnitus, vasculitis, or aortic insufficiency.

DRY EYE SYNDROME

Signs and Symptoms

Dry eye syndrome may occur in a wide range of individuals,

although it is more frequently seen in women, the elderly, and
those with connective tissue disorders (e.g., rheumatoid
arthritis, Sjögren's syndrome). Patients with dry eye commonly
present with complaints of ocular irritation or discomfort. As

Generalized injection associated with

moderate dry eye.
the name implies, dryness is the most frequently cited problem; patients may further report
itching, burning, or a "sandy/gritty" foreign body sensation. Symptoms may be exacerbated by
poor air quality, low humidity or extreme heat, and tend to be more prominent later in the day.
Occasionally, patients will report excess lacrimation, or epiphora, in association with the
discomfort.

Upon gross inspection, the majority of these patients demonstrate a relatively white and quiet
eye. However, key slit lamp findings may include a meager tear meniscus at the lower lid, as well
as a reduced tear break-up time (TBUT), generally less than ten seconds. Sodium fluorescein
staining may be evident as punctate epithelial keratopathy from the interpalpebral region to the
lower third of the cornea. In more severe cases, rose bengal or lissamine green staining of the
cornea and/or conjunctiva may be seen in the same area. Filaments, which are tags composed of
mucus, epithelial cells and tear debris, may also stain with these vital dyes.

Additional clinical tests for dry eye syndrome are numerous. Tear volume assessment is used
quite commonly, and may be ascertained by use of Schirmer tear test strips or the Zone-Quick
test. Dimin-ished "wetting" of these test media over a set period of time (five minutes for the
Schirmer and 15 seconds for the Zone-Quick test) is indicative of tear volume deficiency, a form
of dry eye syndrome. Another device, the Keeler Tearscope, utilizes interferometry to evaluate
the thickness of the tear film components, particularly the lipid layer. More involved and invasive
procedures, including tear film osmolarity, lysozyme analysis, lactoferrin assay, and impression
cytology, may be useful in quantifying dry eye for research purposes, but they are hardly practical
for routine clinical diagnosis.

Pathophysiology

Dry eye syndrome has traditionally been viewed as a

quantitative or qualitative reduction in the precorneal
tear film, with a multitude of etiologies and
contributory factors. The condition tends to be
categorized as either "tear deficient" or "evaporative,"
based upon a comprehensive classification scheme
that was developed in 1995.1 Those conditions that
contribute to diminished tear production, such as
Sjögren's syndrome or lacrimal gland disease, Negative corneal staining from surface disease in
constitute the tear- deficient variety. Conditions dry eye.
involving mucin or lipid deficiencies (e.g., Stevens-Johnson syndrome or blepharitis), irregular
ocular surface topography, altered blink reflex, or other surface disorders comprise evaporative
dry eye. Other contributory factors may include contact lenses, low environmental humidity, and
high altitude.

Over the last several years, a great deal of research has been conducted in the area of dry eye,
revealing startling new information. Of the more intriguing theories is that dry eye may be the
result of an inflammatory process within the cornea and/or lacrimal glands.24 This is supported by
the fact that pro-inflammatory cytokines and activated T cells have been identified in the lacrimal
glands of both Sjögren's and non-Sjögren's patients.5,6 In addition, moderate to severe dry eye
states have been seen to respond favorably to treatment with corticosteroids.7 On another front,
researchers have shown a significant link between androgens and dry eye.8,9 Apparently, these
sex hormones may help regulate homeostasis of the tear secretion process. Women who take
hormone replacement therapy with estrogen have an increased incidence of dry eye, possibly
due to suppression of endogenous androgens by increased estrogen levels.10,11

Management
Historically, management of dry eye syndrome has been aimed at replenishing the eye's moisture
and/or delaying evaporation of the patient's natural tears. The first line of defense typically
involves the use of ophthalmic lubricants ("artificial tears"). The purpose of these agents is to
alleviate symptoms and, in some cases, to promote healing of the ocular surface epithelium. A
great deal of diversity exists within this market, and practitioners should familiarize themselves
with the various options (see "Overview of New Dry Eye Products," on page 34A). In general,
artificial tears may be used as frequently as necessary, although some are only indicated for qid
use. When beginning therapy, they should be dosed frequently (at least every hour), and then
tapered based upon patient response and compliance.

Patients who do not respond to palliative therapy may require more substantial treatment in the
form of topical and/or oral pharmaceutical agents. The immunomodulatory agent Restasis (0.05%
cyclosporine A ophthalmic emulsion, Allergan) has recently been approved by the U.S. FDA "for
patients with keratoconjunctivitis sicca ... whose tear production is presumed to be suppressed
due to ocular inflammation." Although this topical drug may require bid dosing for up to six
months to achieve maximum efficacy, it has been shown to ameliorate symptoms in up to 44% of
patients and improve basal tear production (as demonstrated by Schirmer testing) in up to 59% of
patients.12

Oral medications and nutritional supplements have been utilized with success for patients with
blepharitis and meibomian gland disease, significant causes of evaporative dry eye syndrome.
The use of oral tetracycline therapy (e.g., doxycycline 100mg bid x six to 12 weeks) may be
beneficial in patients who fail to improve with lubricating drops and lid hygiene. Also, the use of
oral omega-3 fatty acid supplements has been suggested as a less invasive way to improve
meibomian gland function and tear stability.13

Lacrimal occlusion with punctal or intracanalicular plugs offers a different management strategy
for dry eye, essentially preventing drainage of the tear film and maximizing contact duration with
the ocular surface. While the theory is sound, a significant percentage of plugs may be
spontaneously expelled, and it has been noted that many patients notice a subjective decrease in
improvement of symptoms with the plugs over time.14,15 Some individuals have actually cautioned
against occlusion therapy in many cases, citing the new inflammatory theories of dry eye; they
suggest that the use of punctal plugs actually creates a "cesspool" of cytokines and promotes,
rather than alleviates, damage to the ocular surface.16

Patients with keratoconjunctivitis sicca (KCS), a more severe form of dry eye, may not respond to
any topical therapy. Often, these patients benefit from oral secretagogues such as Salagen
(pilocarpine HCl 5 mg, MGI Pharma) and Evoxac (cevimeline HCl 30 mg, SnowBrand
Pharmaceuticals). These muscarinic agonists stimulate non-selective secretion from exocrine
glands via autonomic pathways, resulting in enhanced tear production. Typically these agents are
used for xerostomia (dry mouth) associated with Sjögren's syndrome or certain forms of cancer.
They are utilized by some physicians for advanced KCS; however this is not currently an FDA-
approved application of these drugs.

Clinical Pearls

• The symptoms of dry eye syndrome tend to be quite variable. Often, patients seem to be
more symptomatic than their clinical signs would indicate. Astute clinicians realize that
the diagnosis of dry eye is more often based on subjective complaints than on ocular
inspection.
• Many common systemic drugs can transiently decrease lacrimal secretions, creating or
exacerbating a dry eye state. These may include antihistamines, oral contraceptives,
beta-blockers, diuretics, phenothiazine antianxiety preparations, many antidepressants
and atropine derivatives.
 • Before initiating any form of therapy, practitioner and patient alike must understand one
basic tenet of dry eye management: namely, that this is a chronic disease, marked by
exacerbations and remissions. The only way for patients to achieve control of their
symptoms and discomfort is through active participation in the prescribed treatment
regimen and periodic reevaluation. There is no "magic bullet" cure, and appropriate care
requires patience, perseverance and a willingness to try new (and sometimes
unconventional) options.

CORNEAL ABRASION
Signs and Symptoms

Corneal abrasion is one of the common clinical entities that

present to the optometric practice. Patients usually present with
some or all of the following: acute pain, photophobia, lacrimation,
bleph-arospasm, foreign-body sensation, blurry vision and a
history of contact lens wear or being struck in the eye.111
Biomicroscopy of the injured area often reveals diffuse corneal
edema and epithelial disruption. In severe cases, when edema is
excessive, folds in Descemet's membrane may be visible. Cobalt
blue light inspection, following the instillation of sodium fluorescein
dye, will illuminate the denuded epithelium. The newly created
wound appears as a bright green area compared to the rest of the
cornea because the dye accumulates in the divot, adding
density.3,5,10

Pathophysiology
Corneal abrasion without
fluorescein.
The cornea has five distinct layers. Below the tears lies the corneal
epithelium. The corneal epithelium is actually composed of three tissues: the stratified surface
epithelium, the wing cell layer, containing the corneal nerves and the mitotically active basement
membrane. Below the epithelium is the Bowman's membrane (a structure designed to prevent
penetrating injuries), 250 lamellar sheets of stroma, Descemet's membrane, and finally the
endothelium.

There are two categories of corneal abrasion; superficial, not involving Bowman's membrane and
deep, penetrating Bowman's membrane, but not rupturing 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.5 Lesions that are purely epithelial often heal
quickly and completely without scarring. Lesions that extend below Bowman's membrane
possess an increased risk for leaving a permanent opacity.5 Recent data suggests that the
integrity of the basement membrane following the injury is a deciding factor in determining the
regenerative character of the corneal repair.7

For years contact lenses have remained at the top of the list of consumer goods known to
perpetrate ocular injuries. Further, ulceration following contact lens-induced corneal abrasion has
been recognized and demonstrated as a secondary phenomenon to suspect compliance, care
and lens cleanliness.8 In one study, ulcers were found only in corneas that were scratched with
contact lenses colonized by viable S. aureus.8 Bacteriologic examination of lenses at the time of
the event demonstrated the association.8
Management

Treatment for corneal abrasion begins with history. The time, place and activity surrounding the
injury should be recorded for both medical and legal purposes.
Visual acuity (VA) should be recorded before any procedures
or drops are given, if possible. If the blepharo-spasm is
sufficiently intense to preclude an acuity measurement, one
drop of topical anesthetic from a recently open bottle can be
administered. The VA should be measured immediately
thereafter. The eye examination should proceed in a logical
fashion from external adenexa to funduscopic examination.
The eyelids should be everted and fornicies scrutinized to rule Corneal abrasion with fluorescein
out the presence of foreign material. Fluorescein dye (without staining.
anesthetic) should be instilled to identify the corneal defects. The Seidel test (painting of the
wound with dye observing for aqueous leakage) is used to uncover full-thickness injuries. The
abrasion should be documented for size, shape, location and depth. Any anterior chamber
reaction should be observed and noted as well. A dilated examination should be completed to
rule out posterior effects from the trauma.

Medical treatment is initiated by using adequate cycloplegia (the potency of which should be
determined on a case-by-case basis) and topical antibiotics such as Polytrim (polymyxn B and
trimethoprim, Allergan), gentamicin or Tobrex (tobramicin, Alcon) or a fluoroquinolone (Vigamox,
Zymar). Bed rest, inactivity and over-the-counter analgesics can be used to quiet acute pain. In
cases where pain is severe, topical nonsteroidal anti-inflammatory medications (Voltaren or
Acular, qid) or a thin, low water content bandage contact lens can be prescribed.16, 9, 10, 11

Pressure patching is no longer considered standard-of-care.1,2,46,10 Researchers examined patients

with corneal abrasion: 17 with an eye patch and 18 with no eye patch. There was no significant
difference in percent healing between the two groups, even when adjusted for age and initial
abrasion size. Consistent with the data of others, pressure patching for corneal abrasions
provides no benefit.10 Patching must always be avoided in patients who wear contact lenses due
to the threat of microbial keratitis. Patients should be reevaluated every 24 hours until the
abrasion
is reepithelialized.15

Clinical Pearls

• To prevent recurrent erosion and reduce corneal edema, a hypertonic solution or

ointment may be prescribed along with the other medications or after reepithelialization
has occurred.5
• In cases where excess epithelium impairs regrowth, a cotton-tipped applicator saturated
with anesthetic may be used to debride loose tissue.5
• When significant secondary uveitis is present, topical steroids may be required.
• Worsening subepithelial infiltration may be a sign of infection. Lesions such as these
should be considered vision threatening, warranting immediate treatment with
fluoroquinolone antibiotic drops and consideration for culture.3

OVERVIEW OF NEW DRY EYE PRODUCTS

FOR MANY YEARS, there were only two options for managing dry eye syndrome: either put
more moisture into the eye, or prevent the moisture already present from evaporating too quickly.
Ophthalmic lubricating solutions, more commonly known as artificial tears, have remained the
mainstay of dry eye therapy since their introduction in the 1940s.1 Freeman introduced the first
silicone punctal plug in 1975,2 and other devices to prevent surface evaporation (e.g. Moist Eye
moisture panels from EagleVision) have joined the ranks over the years, but these modalities
have never been able to supplant artificial tear therapy from its #1 position.

A cursory review of an online health product service (www.drugstore.com) reveals over 50 distinct
items when the term "artificial tears" is entered in the search engine! With so many products to
choose from, it can be frustrating and intimidating for both patients and practitioners to know
which option to select. The following is a review of some of the more recent products introduced
for therapy of dry eye syndrome.

Trends in Artificial Tears

Despite their popularity and success, two significant difficulties still exist with artificial tears. The
biggest issue is duration of action; patients frequently report only fleeting relief (on the order of
five to 10 minutes) after instillation of many tear supplements. Also of concern is the addition of
preservatives in many artificial tears, which can be a significant source of toxicity, particularly
when these preparations are used frequently. Therefore, manufacturers have begun producing
thicker, more viscous agents that increase corneal contact time without blurring vision. Examples
of such products include Refresh Liquigel (Allergan), GenTeal Gel (Novartis), TheraTears Liquid
Gel (Advanced Vision Research), and Systane (Alcon). Also, manufacturers have introduced
several preservative-free solutions and "disappearing preservatives" to address the issue of
toxicity. Virtually every line of dry eye products includes a preservative-free version (e.g., Tears
Naturale PF, Hypotears PF, etc.), but only three product lines contain preservatives that break
down soon after instillation. These include: GenTeal (Novartis, preserved with GenAqua, or
sodium perborate), Tears Again (Cynacon/Ocusoft, preserved with Dissipate), and Refresh Tears
(Allergan, preserved with Purite).

Nature's Tears

In mid-2002, a small company based in Oregon launched a unique product that has captured the
interest of many exhibit hall attendees. Nature's Tears (Bio-Logic Aqua Technologies) is
described by the manufacturer as an all natural moisturizing mist for the eyes consisting simply of
tissue culture grade water with no preservatives or propellants. Rather than being instilled as a
drop, Nature's Tears is sprayed toward the eyes from a distance of 12 to 18 inches. The premise?
Artificial tears flood the ocular surface, washing away the lipid and mucin layers and depleting
normal enzymes, claims the manufacturer. However, Nature's Tears mist allows for replenishing
of the aqueous component without disturbing the other tear layers. This is an intriguing theory,
and the product possesses a significant novelty factor. However, there is a lack of significant
prospective studies demonstrating that this product is any more effective than other artificial tear
supplements.

Endura

In the summer of 1999, the FDA Ophthalmic Drugs Subcommittee advisory panel unanimously
recommended not to approve Allergan's formulation of topical cyclosporine for the treatment of
keratoconjunctivitis sicca. One of the reasons cited was that the solution vehicle showed very
similar efficacy to the drug itself, and hence there was no significant difference between the
controls and the study group. Undaunted, Allergan decided to manufacture this unique vehicle, an
emulsion of castor oil and lubricants in an aqueous solution, and market it directly to the public as
an over-the-counter product. In the fall of 2002, Refresh Endura was launched.

According to Allergan, Endura is the first lubricant eye drop for dry eye that treats all three layers
of the tear film. It is preservative-free and packaged in single-use, disposable vials. Controlled
clinical trials with Endura showed enhanced fluorescein tear break-up time, as well as diminished
symptoms of dryness and irritation in patients using the solution two to four times daily over 90
days. Clinical practice has shown it to be an excellent and well-tolerated solution, particularly
suited for patients with lipid deficiencies secondary to meibomian gland dysfunction.

Systane

In early 2003, Alcon introduced a unique artificial tear product. Systane, which utilizes the
demulcent technology of hydroxypropyl (HP) guar, increases in viscosity after contacting the
ocular surface. This change is based on pH value. Systane is a liquid in the bottle at a pH of 7.0,
but when placed in the eye (which has a pH of ~7.4), a chemical reaction occurs. HP guar binds
to the ocular surface and simultaneously crosslinks with borate ions in the solution, forming a
network with a gel-like consistency. The result is a more viscous ocular lubricant that, according
to Alcon, provides extended relief of dry eye symptoms and generates a protective coating on the
ocular surface. In theory, this coating serves as a temporary corneal bandage, allowing the
epithelial cells to heal and reestablish healthy microvilli and a normal glycocalyx.

In a randomized, controlled clinical trial, dry eye patients receiving Systane four times daily for six
weeks showed a statistically significant reduction in surface staining, dryness and foreign-body
sensation, as well as increased tear break up time.3,4 Mild blurring for 30 seconds after instillation
was the most significant adverse effect. Personal experience with Systane has shown it to be an
outstanding choice for patients with moderate to severe dry eye who are not ameliorated with
normal viscosity tear solutions. It is also excellent for managing minor corneal trauma or exposure
keratopathy.

Restasis

In December 2002, the FDA approved Restasis (0.05% cyclosporine ophthalmic emulsion) for the
treatment of keratoconjunctivitis sicca, making it the first commercially available pharmaceutical
therapeutic agent for the treatment of dry eye. This topical solution is classified as an
immunomodulatory agent by the manufacturer (Allergan), and is approved "for patients with
keratoconjunctivitis sicca...whose tear production is presumed to be suppressed due to ocular
inflammation."

In clinical studies, Restasis was shown to ameliorate symptoms in up to 44% of patients and
improve basal tear production (as demonstrated by Schirmer testing) in up to 59% of patients
after six months of treatment.5 Additionally, a reduction in conjunctival T-lymphocyte infiltration
was noted after six months of cyclosporine therapy.6

Allergan heralds Restasis as the first drug proven to effectively treat a cause of dry eye disease,
rather than only temporarily alleviate symptoms. But although this product has yielded good
results in clinical trials, practitioners have been somewhat reluctant to actively prescribe Restasis
for several reasons. First, many are confused as to precisely which dry eye patients will benefit
from this therapy. Second, ocular burning has been reported as an adverse event in up to 17% of
individuals utilizing the drug.5 Third, the time frame of six months may seem irrationally long for
some practitioners and patients to observe improvement in the disease course (even though
many patients experience improvement after only a few weeks). Finally, the retail cost of Restasis
is somewhat expensive as compared to conventional therapy, on the order of $80 to $100 per
month. While these issues cannot be ignored, the fact remains that Restasis may offer great
potential benefit to many of our patients. Practitioners need to remain open minded and
personally evaluate this product on at least a few patients before reaching the conclusion that it is
too slow, too uncomfortable or too expensive. Restasis is prescribed on a bid basis.

Therapies on the Horizon

More products remain under investigation for the treatment of dry eye syndrome. Diquafosol
tetrasodium, a topical agent referred to as INS365 Ophthalmic by Inspire Pharmaceuticals, has
been shown to activate P2Y2 receptors in the mucosal cells of the palpebral conjunctiva.7,8 These
receptors are believed to regulate a variety of cellular responses.

When used topically on the ocular surface, INS365 has been shown to pull salt, water and mucin
from conjunctival cells, effectively creating an artificial tear comprised of purely endogenous
components.7 Inspire Pharmaceuticals filed a new drug application for INS365 in June 2003, and
received an approvable letter from the FDA on December 22, 2003. A launch of this product is
anticipated sometime in 2004.

Still in clinical trials is 15(S)-HETE (15-hydroxyeicosatetraenoic acid) from Alcon Laboratories.

Like INS365, this product is best described as a secretagogue, in that it induces secretions from
bodily tissues. Specifically, when instilled in the eye, 15(S)-HETE stimulates production of the
glycoprotein Muc1.9 Muc1 is an important component of the tear mucin layer; enhancement of
this element may help to alleviate corneal injury and restore corneal integrity in dry eye patients.

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
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

• Choroidal neovascularization can occur five years after the initial trauma.
• Sub-retinal hemorrhage from choroidal neovascularization is the most common cause of late
vision loss.
• 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.

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
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

• 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."
• 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.

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.

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.

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.
• 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.

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.
(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.

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 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.

Clinical Pearl

• 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.

DIABETIC RETINOPATHY
SIGNS AND SYMPTOMS
A microvascular disease that primarily affects the capillaries,
diabetes mellitus affects the eye by destroying the vasculature in the
conjunctiva, retina and central nervous system. Patients may present
with histories of long-standing injected bulbar conjunctivae along
with systemic complaints of weight loss despite larger than normal
appetite (polyphasia), abnormal thirst (polydypsia) and abnormally
frequent urination (polyuria).

Fluctuating visual acuity secondary to unstable blood sugar is a

common ocular sign. Swelling within the crystalline lens results in
large sudden shifts in refraction as well as premature cataract
formation. Changes in visual acuity will depend upon the severity and stage of the disease.

In the retina, weakening of the arterioles and capillaries may result in the characteristic appearance of
intraretinal dot and blot hemorrhages, exudates, intraretinal microvascular abnormalities (IRMA)
microaneurysms, edema and cotton wool infarcts. Proliferative diabetic retinopathy is the result of severe
vascular compromise and is visible as neovascularization of the disc (NVD), neovascularization elsewhere
(NVE) and neovascularization of the iris (NVI, or rubeosis irides). Neurological complications include
palsies of the third, fourth and sixth cranial nerves as well as diabetic papillitis and facial nerve paralysis.

PATHOPHYSIOLOGY
Diabetes mellitus is a genetically influenced group of diseases that share glucose intolerance. It is
characterized as a disorder of metabolic regulation as a result of deficient or malfunctioning insulin or
deficient or malfunctioning cellular insulin receptors.

Biochemistry involving the formation of sorbitol plays a role in the destruction of pericytes, which are cells
that support the vascular endothelium. As the supportive pericytes perish, capillary endothelium becomes
compromised, resulting in the vascular leakage of blood, protein and lipid. This, in combination with
thickened, glucose-laden blood, produces vascular insufficiency, capillary nonperfusion, retinal hypoxia,
altered structure and decreased function. The formation and release of vasoproliferative factors which play
a role in the genesis of retinal neovascularization are poorly understood.

MANAGEMENT
When you suspect ocular sequelae of diabetes mellitus in an undiagnosed individual, either you or the
patient's physician should order a fasting blood glucose (FBS), glycosylated hemoglobin or oral glucose
tolerance test (OGTT).

Most non-vision threatening sequelae of diabetes resolve spontaneously over the course of weeks to months
following medical control. In cases where there are large refractive changes, patients may require a
temporary spectacle prescription until the refraction stabilizes. The most important element of

MANAGEMENT is education so that patients are informed that they may eventually need to change their
spectacle lenses.

When retinopathy threatens the macula or when new blood vessels proliferate, refer for laser
photocoagulation. The Diabetic Retinopathy Study (DRS) has conclusively proven that panretinal
photocoagulation was successful in reducing the risk of severe vision loss in high risk patients. It defined
the high risk characteristics as: (1) Neovascularization of the optic disc (NVD) one-quarter to one-third of a
disc diameter in size and (2) Neovascularization elsewhere (NVE) with any vitreous hemorrhage.

If the patient exhibits either of these high risk characteristics, refer him or her to a vitreoretinal specialist.

The Early Treatment of Diabetic Retinopathy Study (ETDRS) has shown that focal/grid laser
photocoagulation reduced the risk of moderate vision loss in patients with clinically significant macular
edema, defined as: (1) retinal thickening at or within 500 microns (one-third of a disc diameter) of the
center of the foveola, (2) exudate at or within 500 microns of the center of the foveola only if associated
with retinal thickening, or (3) an area of retinal thickening one disc diameter or greater in size, within one
disc diameter of the foveola.

If you observe any of these signs, regardless of the acuity, refer the patient to a retinal specialist. Referral is
also indicated if you suspect clinically significant macular edema but are having difficulty visualizing the
macula or edema.

CLINICAL PEARLS

• Clinically significant macular edema is unrelated to acuity and can exist in the presence of 20/20
vision. It can only be identified through observation using stereoscopic indirect biomicroscopy
(60D, 78D, 90D Hruby or three-mirror lens).
• Fluorescein angiography is only used for treatment. It identifies the areas of leakage that require
focal grid laser photocoagulation. With respect to diabetes, it is not a tool for diagnosis.
 Angiography is not required for treating proliferative disease since PRP does not require precise
aiming of the laser.
• The development of diabetic retinopathy is time-dependent. Even in the face of optimal blood
sugar control, patients with long-standing disease can be expected to eventually develop some
form of retinopathy.

POSTERIOR VITREOUS DETACHMENT

SIGNS AND SYMPTOMS
The patient, usually over the age of 50, will present with a sudden
onset of floaters. There is usually one floating spot that is especially
large and troublesome to the patient and serves as the impetus to
seek immediate care. There may also be associated photopsia if the
patient is experiencing vitreoretinal traction. If the patient presents
with multiple floaters, there may be an associated vitreous
hemorrhage, especially if there is an associated reduction in visual
acuity. Patients who report diffuse floaters during routine
examination usually are suffering from benign vitreous syneresis
and not posterior vitreous detachment.

PATHOPHYSIOLOGY
The vitreous is comprised of collagen fibrils and glycoaminoglycans, supported by hyaluronic acid
molecules. With aging, reduction in hyaluronic acid causes loss of support to the collagen. The vitreous
may collapse, with detachment of the posterior hyaloid face from the optic disc. This usually is observable
ophthalmoscopically as an annulus floating in the vitreous over the posterior pole. As the vitreous detaches
peripherally, areas of vitreoretinal adhesion may result in a tear in the sensory retina with the ensuing
possibility of a rhegmatogenous retinal detachment. If the tear bridges a blood vessel, a vitreous
hemorrhage ensues.

MANAGEMENT
A PVD found asymptomatically on routine examination is benign, but requires monitoring yearly. A
patient who presents with a sudden onset PVD without retinal breaks or hemorrhage requires repeat
peripheral examination in six weeks, as the risk of retinal complications is highest within the six weeks
following vitreous detachment. If no retinal breaks are seen at that point, routine yearly examination is all
that is needed. Prophylactically treat any fresh breaks associated with a new PVD immediately with
photocoagulation or cryoretinopexy.

CLINICAL PEARLS

• Occasionally, a new PVD will present with a small amount of pre-retinal or vitreous hemorrhage
without an observable retinal break. This patient needs a detailed peripheral exam using scleral
indentation as well as Goldmann and/or Volk lens evaluation.
• If no retinal breaks are initially detected, the patient needs a repeat evaluation every two weeks for
six weeks to look for an occult break not originally found. If you do not observe any breaks after
six weeks, the blood resulted from torn retinal or disc capillaries, and the patient is out of
immediate danger.

RETINAL VEIN OCCLUSION

SIGNS AND SYMPTOMS
The patient will usually be elderly, often with a history of systemic
diseases such as diabetes and hypertension. The patient may be
asymptomatic, but often will complain of sudden painless unilateral
loss of vision and/or visual field, and may complain of a sudden
onset of floating spots or flashing lights. Acuity may range
anywhere from 20/20 to finger counting. If vision loss is severe,
there may be a relative afferent pupillary defect.

Ophthalmoscopically, there will be retinal edema, superficial

hemorrhages, disc swelling, cotton wool spots, and tortuous and Ischemic Central Retinal Vein
dilated retinal veins. If there is a central retinal vein occlusion, these Occlusion
findings will encompass all four retinal quadrants. A hemi-central
retinal vein occlusion will involve only the superior or inferior half
of the retina. A branch retinal vein occlusion will present with
findings in only one quadrant, usually supero-temporal, with the
apex of the hemorrhage at an arteriovenous crossing.

The hemorrhaging may be so severe that all features of the

underlying retina are obscured. Multiple cotton wool spots indicate
retinal ischemia and capillary non-perfusion. Anterior and posterior
segment neovascularization may occur later in the disease.

PATHOPHYSIOLOGY
The etiology of central and hemi-central retinal vein occlusion is an
obstruction of the central retinal vein, or one of the vein's two Non-ischemic Hemi-central Retinal Vein
trunks, as it constricts through the lamina cribrosa. The cause is Occlusion
obscure, but may involve abnormal blood flow or blood constituents,
atherosclerosis, vessel anomalies or a combination of these factors.

The etiology of a branch retinal vein occlusion is an

arteriolosclerotic arteriole crossing and constricting the underlying
venule. This will result in leakage from the capillary beds draining
into these vessels. The capillary beds may be irreversibly damaged
by this leakage, resulting in perpetual non-perfusion of the retinal
tissue. If a significant area of capillary non-perfusion is present, then
the occlusion is considered ischemic.

Loss of retinal capillary beds with subsequent retinal non-perfusion

will lead to retinal hypoxia and the subsequent release of Non-ischemic Branch Retinal Vein
vasoproliferative substance. Vasoproliferative factors will then Occlusion
stimulate the proliferation of neovascularization from nearby viable
capillary beds.

In branch and hemi-central occlusions, neovascularization will most

often form on the optic disc or adjacent retina and can lead to
vitreous hemorrhage and tractional retinal detachment. In central
retinal vein occlusions, the closest viable capillary network from
which neovascularization will form is typically the posterior iris.
This can lead to rubeosis irides and neovascular glaucoma. In all
cases of venous occlusion, the main cause of vision decrease is
macular edema. However, if retinal capillary non-perfusion involves
the perifoveal region, then vision is dramatically and irreversibly
lost.
MANAGEMENT
Fluorescein angiography, long held to be the gold standard in
assessing retinal vascular disease, has questionable use in vein
occlusions. It is not indicated initially, as the fresh hemorrhage will
block transmission and reveal no useful information, but later in the
disease it will provide information about retinal capillary perfusion
and whether or not the occlusion is ischemic and thus more likely to
foster neovascularization. New research indicates that ischemic
retinal vein occlusions do not benefit from prophylactic PRP;
withhold this procedure until the patient develops frank
neovascularization of the iris, disc or retina.

Monitor the patient monthly with serial ophthalmoscopy, fundus

photography and goniscopy until you see resolution. If the patient
has a hemi-central or branch retinal vein occlusion and vision is
below 20/40 due to macular edema, the patient will benefit from
focal laser photocoagulation anywhere between three and 18 months
after the occlusion's onset. Central retinal vein occlusion patients
with vision reduction due to macular edema do not benefit from the
proceudre, according to new research.

Due to the association of systemic disease with vein occlusions, co-

manage the patient with an internist. Tests to be ordered include:
blood pressure, fasting blood glucose, lipid and cholesterol studies,
FTA-ABS, complete blood count with differential, sickle dex (if the
patient is African-American), anti-nuclear antibodies, angiotensin
converting enzymes, and viscosity studies.

CLINICAL PEARLS

• Ischemic vein occlusions are the only vein occlusions that

will likely develop neovascular complications, and they
account for only one-third of all occlusions.
• Ischemic vein occlusions typically present with acuity
worse than 20/200. Those eyes with initial acuity better
than 20/200 are at very low risk of developing severe,
permanent vision loss, and are likely to resolve.
• Ischemic occlusions are likely to present with a relative
afferent pupillary defect. If not, then it is likely non-
ischemic.

RETINAL ARTERY OCCLUSION

 Branch Retinal Artery Occlusion
Retinal Artery Occlusion

SIGNS AND SYMPTOMS

The patient, usually between the ages of 50 and 80, will present with a sudden, painless, unilateral loss of
vision and/or visual field. Acuity may be as low as hand motion. The patient often has significant systemic
illness such as hypertension and/or diabetes. There will be a relative afferent pupillary defect in the
involved eye.

Ophthalmoscopically, you'll see a pale, milky, edematous retina with attenuated arterioles and a cherry-red
macula if the entire central retinal artery is occluded. If a cilioretinal artery is present, there will be an area
of perfusion from the optic disc to the macula. An embolus may be visible in the vasculature on the disc. If
a branch retinal artery is involved, an embolus will be visible in the vessel with ischemia and infarct
appearing distal to the occlusion.

PATHOPHYSIOLOGY
The main cause of retinal arterial occlusions is an embolism lodging in the central retinal artery where it
constricts to pass through the lamina cribrosa, or in a smaller branch arteriole. The embolism may be
comprised of aggregated fibrin and platelets arising from an ulcerated vessel wall thrombus, cholesterol
from an ulcerated carotid artery plaque, or calcium from cardiac valvular disease.

Abnormal cardiac rhythms may allow blood to coagulate and form emboli which may also reach the retinal
vasculature. Neovascularization is not common with either central or branch artery occlusions, but if it does
occur, it will do so rapidly, with rubeosis forming approximately four weeks after the occlusion. Between
two and 10 percent of central retinal artery occlusions are caused by thrombus formation from giant cell
arteritis (GCA). If the underlying cause of the central retinal artery occlusion is GCA, there may be a rapid
progression to bilateral vision loss if left untreated.

MANAGEMENT
Traditionally, central retinal artery occlusion has been considered an emergency. It was felt that, if the
embolus could be dislodged within 90 minutes of occlusion, vision could be potentially salvaged with the
retina being re-perfused. To this end, various methods have been employed to reduce resistance on the
artery or dilate the artery to induce the embolus to dislodge.

Common methods employed included breathing into a paper bag to increase blood carbon dioxide levels
and induce vasodilation, digital globe massage, paracentesis, and carbonic anhydrase inhibitors to reduce
intraocular pressure and decrease vascular resistance to flow. Most practitioners would attempt these
measures if the occlusion were less than 24 hours old. While there is anecdotal evidence that these
measures have sporadically resulted in vision returning, a large study showed that the average final visual
outcome in patients with embolic central retinal artery occlusion treated with heroic measures compared to
those untreated was only one-quarter line improvement in Snellen acuity.
Patients with arterial occlusion have significant systemic illness, namely hypertension, atherosclerosis or
diabetes. These patients are at extreme risk for cardiovascular disease and myocardial infarction. For this
reason, these patients need prompt referral to a cardiologist for complete evaluation. Medical testing should
include blood pressure evaluation, EKG, fasting blood glucose, lipid and cholesterol levels, and
hyperviscosity studies. Patients with central retinal artery occlusion over the age of 60 need an immediate
erythrocyte sedimentation rate (ESR) to examine for the possibility of giant cell arteritis. Fluorescein
angiography is generally not indicated.

CLINICAL PEARLS

• Traditional heroic measures to salvage vision generally do not produce significant changes in the
patient's vision.
• These patients have a significantly reduced survival rate, and the main cause of mortality is
cardiac. Therefore, prompt referral to a cardiologist is indicated.
• Central retinal artery occlusion may be caused by GCA; if undetected, the patient can develop
severe, bilateral vision loss

RETINITIS PIGMENTOSA
SIGNS AND SYMPTOMS
Patients with retinitis pigmentosa (RP) may present with varying
symptoms. The onset is often gradual and insidious, and many
patients fail to recognize the manifestations of this condition until it
has progressed significantly. When patients do report symptoms, they
commonly include difficulty with night vision (nyctalopia) as well as
loss of peripheral vision.

Many patients with RP also experience photopsiae as the disorder

progresses; typically they report small flashes of light or a twinkling,
shimmering sensation in the midperipheral or peripheral field. These
are believed to represent aberrant electrical impulses from the degenerating retina.

Central visual acuity is generally not affected until the very late stages of RP, although variants have been
encountered that cause devastating macular compromise early in the disease course (e.g., X-linked
recessive RP). Color vision is typically remains intact as long as visual acuity is better than 20/40.

Attenuation of the retinal arterioles is the earliest observable sign in RP. Retinal pigmentary changes occur
in the form of fine mottling or granularity with surrounding areas of atrophy. Later, stellate pigment
hyperplasia may be noted at perivascular locations in the midperipheral retina. These hyperplastic
formations are often referred to as "bone spicules."

As the disorder progresses, general atrophy of the RPE and choriocapillaris ensues, exposing the larger
choroidal vessels. The optic nerve head is often normal in early RP, but may demonstrate a waxy yellow or
pale appearance later. RP has a strong correlation with acquired optic disc drusen. The macula, like the
optic nerve, is usually unaffected in the early stages, but in some forms of RP may demonstrate preretinal
gliosis ("cellophane maculopathy"), cystoid macular edema or focal RPE defects. Additional findings in RP
include pigment cells in the vitreous ("tobacco dust sign"), posterior vitreous detachment and posterior
subcapsular cataracts.

Most patients with retinitis pigmentosa are myopic, and many have keratoconus as well. Electrodiagnostic
testing in RP shows a significantly diminished scotopic ERG as well as an abnormal EOG and dark
adaptometry.
PATHOPHYSIOLOGY
Retinitis pigmentosa is believed to stem from a genetic defect, which leads to a disturbance in the retinal
pigment epithelium (RPE) and the breakdown of the photoreceptors' outer segment disc membranes. The
resultant accumulation of metabolic by-products disrupts retinal function, and manifests as lipofuscin
deposition, retinal gliosis, photoreceptor loss, choriocapillaris occlusion and RPE hyperplasia. These RPE
changes compromise the blood-retina barrier, resulting in subretinal leakage and macular edema in later
stages. Because the affected photoreceptor cells in most cases are rods, the patient typically experiences
visual difficulty under dark conditions, as well as peripheral field constriction.

There are many forms of retinitis pigmentosa, and while most present with similar findings and outcome,
some presentations are atypical. RP may be classified on the basis of inheritance pattern (autosomal
dominant, autosomal recessive, X-linked, simplex, multiplex), age of onset (congenital, childhood onset,
juvenile onset, adult onset), predominant photoreceptor involvement (rod-cone, cone-rod), or location of
retinal involvement (central, pericentral, sectoral, peripheral).

MANAGEMENT
Since there is no known treatment for retinitis pigmentosa, management calls for prompt diagnosis and
subsequent counseling to maintain quality of life.

Always obtain visual fields and electrodiagnostic testing to confirm the diagnosis of RP; order serology if
the diagnosis is unclear or other disorders are suspected.

Most experts recommend a pedigree analysis of patients once RP has been diagnosed. This is critical to
determine the exact inheritance pattern of the patient's condition. Individuals should know the risk for their
progeny or other family members developing the disease.

Recommend genetic counseling to help the patient deal with these issues. Implement low-vision services as
the disorder begins to affect visual function. Field-expansion devices, infrared blocking sun lenses and
contrast enhancing filters may be helpful. Periodic optometric follow-up is also important. Perform visual
fields several times a year, and evaluate for cataract or macular edema at least annually.

CLINICAL PEARLS

• Most patients with RP are diagnosed in the second or third generation of life. Because of the
insidious nature of the disorder, the earliest indicators are often objective findings rather than
subjective complaints. Some presentations are extremely subtle, particularly in the early stages.
Perform a critical evaluation on all patients presenting with complaints of nyctalopia or peripheral
field loss.
• The diagnosis of RP is often based upon appearance, but many "masqueraders" exist, including
rubella retinopathy, syphilitic retinopathy, CMV retinopathy, toxoplasmosis, cancer-associated
retinopathy, retinal drug toxicity secondary to thioridazine, chlorpromazine or chloroquine,
pigmented paravenous retinochoroidal atrophy, and traumatic retinopathy.
• Understandably, the untreatable progressive nature of retinitis pigmentosa is extremely unsettling
for the patient and their loved ones; it is often beneficial to recommend psychological or family
counseling early in the disease.
• Impress upon these patients also that, although they cannot be cured, they still require periodic
examination to assess their status as well as manage their ongoing refractive needs. Also stress the
potential for visual enhancement through low-vision devices and vision rehabilitation.

RETINAL DETACHMENT
 SIGNS AND SYMPTOMS
There are three forms of retinal detachment:

1. Rhegmatogenous retinal detachment (RRD), which results from a

retinal break. The vast majority of rhegmatogenous detachments are
symptomatic, with patients reporting photopsiae, floating spots,
peripheral visual field loss, central blurring of vision or
metamorphopsia.

2. Exudative or serous retinal detachment (ERD), which results from

fluid accumulation under the sensory retina without a retinal break.
Exudative detachments do not generally present with photopsiae but may be associated with moderate
vision loss, metamorphopsia or a visual field deficit.

3. Tractional retinal detachment (TRD), which results from the pull of proliferative fibrovascular vitreal
strands. Tractional detachments are typically asymptomatic unless central vision is threatened, in which
case the patient can suffer severe and abrupt vision loss.

In cases of extensive unilateral retinal detachment, you may observe a relative afferent pupillary defect.
Intraocular pressure may be reduced in eyes with acute retinal detachment.

Ophthalmoscopy in cases of RRD usually reveals a clumping of pigment cells within the anterior vitreous
(Shaffer's sign). There may be an area of white or grayish elevated retina adjacent to the instigating retinal
break. If a significant area of the retina is involved, you may note a milky, lackluster appearance with
undulating retinal folds.

A rhegmatogenous detachment will not change position with changes in body posture, however it may shift
and then return to its original orientation with quick eye movements. Associated findings may include
posterior vitreous detachment and preretinal or vitreal hemorrhage. Retinal pigment epithelial hyperplasia
may be noted in cases of long-standing retinal detachment (pigment demarcation line), and is a good
prognostic feature.

ERD appears clinically as a focal, serous elevation of the retina, which shifts position with changes in
posture and eye movement. The subretinal fluid obeys gravity, always affecting the lowest aspect of the
eye. Ophthalmoscopy reveals a smooth, translucent, dome-shaped protrusion of the retina. There are
usually no hemorrhages, except in cases of associated retinal vasculopathy.

TRD is always associated with vitreal strands and membranes. It appears as a concave, smooth-surfaced
detachment with marginal fibrovascular bands emanating into the vitreous body. It is sometimes difficult to
assess where the necrotic retina ends and the vitreal membranes begin. Very often, this area encircles an
intact posterior pole, resulting in a retinal "pseudo-hole." TRDs are dense and immobile. This motility lends
itself well to ancillary testing with ultrasonography.

PATHOPHYSIOLOGY
All retinal detachments involve the sensory retina dissecting from the underlying pigment epithelial layer
by subretinal fluid. In rhegmatogenous detachments, this fluid is liquefied vitreous, which accesses the
subretinal space via a retinal break. In exudative detachments, the fluid is derived from the choroid, passing
through a defective Bruch's membrane. The origin of the subretinal fluid in tractional detachments is
unknown. Both passive and active movement of subretinal fluid induce progression of retinal detachments,
leading to partial or total loss of vision in some patients.

Retinal breaks are the predisposing factor in patients with rhegmatogenous detachment. These may result
from preexisting conditions or ocular trauma. Some of the more common entities associated with RRD
include lattice degeneration, flap tears, atrophic holes, operculated retinal breaks, and acquired retinoschisis
with both inner and outer holes. As the retinal tissue loses its connection to the RPE, it becomes edematous
and dysfunctional. Without surgical intervention, death of this tissue occurs within 48 to 72 hours.

Exudative detachments are relatively rare, occurring in association with subretinal disorders that damage
the RPE layer. These may include choroidal neoplasms, Vogt-Koyanagi-Harada syndrome, posterior
scleritis, congenital optic disc anomalies (optic pits, morning glory syndrome, etc.), Coat's disease and
uveal effusion syndrome.

Transudation of fluid through the RPE defects causes detachment of the otherwise normal sensory retina.
As the fluid shifts with eye and head movements, the involved portion of the retina changes. This explains
why most patients with ERDs suffer significantly less devastating visual compromise than those with
RRDs or TRDs.

Tractional detachments occur only in proliferative vitreoretinopathies. The most common of these is
proliferative diabetic retinopathy, but many TRDs are associated with ischemic retinal vein occlusions,
sickle cell retinopathy, retinopathy of prematurity, toxocariasis and trauma.

The etiology of TRD involves fibrotic scaffolding of the vitreous along proliferative vascular networks
which induce strong anterior tractional forces through vitreal shrinkage. These forces induce the sensory
retina to separate from the underlying RPE.

Unlike rhegmatogenous or exudative detachments which tend to be abrupt, TRDs are often slow and
insidious, progressing at the same rate as the associated fibrovascular proliferation. Peripheral TRDs are
therefore rarely if ever noticed by the patient. Macular TRDs, on the other hand, tend to be symptomatic,
unless the underlying disease process has already compromised visual acuity.

MANAGEMENT
Patients presenting with an acute onset rhegmatogenous detachment that involves or threatens the macula
warrant immediate retinal specialist consultation. All other fresh RRDs should be repaired within 24 to 48
hours; chronic or long-standing RRDs requiring treatment should be addressed within one week of
diagnosis. While small retinal breaks or atrophic holes may be managed with laser photocoagulation or
cryopexy, true retinal detachments require surgical repair.

Treatment options for RRD include scleral buckling procedures, pneumatic retinopexy and intraocular
silicone oil tamponade. Most practitioners are familiar with scleral buckling procedures, the traditional
surgery for retinal detachment. The retinal tear is first repaired with cryopexy, and the subretinal fluid is
drained via a small scleral incision. Then, under general anesthesia, a soft silicone sponge or hard silicone
band is used to indent the eye at the point of detachment, or to encircle the eye if the detachment is
significant. This explant is sutured into place to reestablish adhesion between the sensory retina and RPE.

In pneumatic retinopexy, an intravitreal gas bubble (usually perfluoropropane, C3F8) serves to reattach the
retina. This technique, performed under local anesthesia, is more common for treating smaller, superiorly
located detachments. Cryopexy is performed at the site of the break, and then the gas is injected into the
vitreal cavity. Careful eye and head positioning are important postoperatively to ensure resolution.

In certain instances, silicone oil tamponade may be favorable to either of these techniques. This procedure
is identical to pneumatic retinopexy except that silicone oil replaces the expansive gas. (Silicone oil
tamponade was actually used prior to the advent of pneumatic retinopexy, however the former has fewer
applications and is therefore done less frequently.) Silicone oil tamponade is most commonly used to repair
RRD resulting from cytomegalovirus infection in AIDS.
Exudative detachments, because of their nature, require intervention less often than do RRDs. ERDs will
usually resolve spontaneously with appropriate management of the underlying condition. This may involve
high-dose steroids in the case of inflammatory disorders, or radiation therapy and/or local resection in the
case of intraocular neoplasms.

Because of their progressive nature, tractional detachments are typically more difficult to manage than
either RRDs or ERDs. For this reason, intervention is often not attempted unless the macula is involved or
threatened. Surgical repair of TRD usually involves pars plana vitrectomy. Silicone oil tamponade is
another popular technique for the treatment of tractional detachments.

CLINICAL PEARLS

• Failure to diagnose retinal detachment remains the second-most-common malpractice claim

against optometrists. All patients presenting with symptoms of retinal detachment or a
predisposing history (peripheral retinal thinning or breaks, blunt ocular trauma, proliferative
diabetic vitreoretinopathy, etc.) must undergo a thorough dilated fundus evaluation, with scleral
indentation where appropriate.
• Refer fresh rhegmatogenous detachments immediately for evaluation and surgical intervention,
particularly if the macula is involved or threatened. In addition, superior detachments present a
greater urgency than do other RRDs, because of the forces of gravity (this rule does not apply to
retinal breaks without detachment, although many practitioners erroneously believe so).
• In cases of long-standing retinal detachment, make patients aware of the permanent nature of the
vision loss. Conservative surgical management may still be indicated for partial or sectoral RRDs,
to secure the remaining retina against the odd chance of ocular trauma and subsequent detachment.
Complete RRDs lasting more than two weeks are usually not treated surgically, as the potential
risks outweigh the benefits.
• Exudative retinal detachments are encountered far less frequently than RRDs, and are often related
to more severe conditions that may need to be co-managed with an ophthalmologist. Tractional
detachments represent the most ominous sequela of proliferative vitreoretinopathies. Again,
ongoing ophthalmologic co-management should be the rule in these cases.

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.