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DISORDERS OF THE EYES & LIDS
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179
1. Optic disk cupping—Optic disk cupping is identified as
an absolute increase or an asymmetry between the two eyes
of the ratio of the diameter of the optic cup to the diameter
of the whole optic disk (cup-disk ratio). (Cup-disk ratio
greater than 0.5 or asymmetry between eyes of 0.2 or more
is suggestive.) Detection of optic disk cupping and associated abnormalities of the retinal nerve fiber layer is facilitated by optical coherence tomography scans.
2. Visual field abnormalities—Visual field abnormalities
initially develop in the paracentral region, followed by
constriction of the peripheral visual field. Central vision
remains good until late in the disease.
3. Intraocular pressure—The normal range of intraocular
pressure is 10–21 mm Hg. In many individuals (about
4.5 million in the United States), elevated intraocular pressure is not associated with optic disk or visual field abnormalities (ocular hypertension). Monitoring for the
development of glaucoma is required in all such cases; a
significant proportion of eyes with primary open-angle
glaucoma have normal intraocular pressure when it is first
measured, and only repeated measurements identify the
abnormally high pressure. In normal-tension glaucoma,
intraocular pressure is always within the normal range.
» Prevention
There are many causes of optic disk abnormalities or visual
field changes that mimic glaucoma, and visual field testing
may prove unreliable in some patients, particularly in the
older age group. Hence, the diagnosis of glaucoma is not
always straightforward and screening programs need to
involve eye care professionals.
Although all persons over age 50 years may benefit
from intraocular pressure measurement and optic disk
examination every 3–5 years, screening for chronic openangle glaucoma should be targeted at individuals with an
affected first-degree relative, at persons who have diabetes
mellitus, and at older individuals with African or Hispanic
ancestry. Screening may also be warranted in patients taking long-term oral or combined intranasal and inhaled
corticosteroid therapy. Screening for chronic angle-closure
glaucoma should be targeted at persons with Inuit or Asian
ancestry.
» Treatment
A. Medications
Medical treatment is directed toward lowering intraocular
pressure, even with normal-tension glaucoma. Prostaglandin analog eye drops are commonly used as first-line therapy because of their efficacy, lack of systemic side effects,
and convenient once-daily dose (except unoprostone) (see
Table 7–2). All may produce conjunctival hyperemia, permanent darkening of the iris and eyebrow color, increased
eyelash growth, and reduction of periorbital fat (prostaglandin-associated periorbitopathy). Latanoprostene bunod
is metabolized into latanoprost and another component
that releases nitric oxide, which increases trabecular outflow. Topical beta-adrenergic blockers may be used alone or
in combination with a prostaglandin analog. The use of
topical beta-adrenergic blockers may be contraindicated in
patients with reactive airway disease or HF. Cardioselective
betaxolol is theoretically safer in reactive airway disease but
less effective at reducing intraocular pressure. Brimonidine
0.2%, a selective alpha-2-agonist, and topical carbonic
anhydrase inhibitors can be used in addition to a prostaglandin analog or a beta-blocker or as initial therapy when
prostaglandin analogs and beta-blockers are contraindicated. All three are associated with allergic reactions. Brimonidine may cause uveitis. Apraclonidine, 0.5–1%,
another alpha-2-agonist, can be used to defer the need for
surgery in patients receiving maximal medical therapy, but
long-term use is limited by adverse reactions. It is more
commonly used to control acute rise in intraocular pressure, such as after laser therapy. The topical agent netarsudil
ophthalmic solution 0.02% (a Rho kinase inhibitor)
increases aqueous fluid outflow through the trabecular
meshwork. Pilocarpine 1–4% is rarely used because of
adverse effects. Oral carbonic anhydrase inhibitors (such as
acetazolamide) may be used long-term if topical therapy is
inadequate and surgical or laser therapy is inappropriate.
Various eye drop preparations combining two agents
(eg, prostaglandin analogs, beta-adrenergic blocking
agents, brimonidine, and topical carbonic anhydrase inhibitors) are available to improve compliance when multiple
medications are required. Formulations of one or two
agents without preservative or not including benzalkonium
chloride as the preservative are preferred to reduce adverse
ocular effects for patients with allergies or severe dry eyes.
B. Laser Therapy and Surgery
1. Open-angle glaucoma—Laser trabeculoplasty is used as
an adjunct to topical therapy to defer surgery for openangle glaucoma; it is also advocated as primary treatment,
especially when compliance with medications is an issue.
Surgical trabeculectomy is generally undertaken when
intraocular pressure is inadequately controlled by medical
and laser therapy, but it may also be used as primary treatment in advanced cases. Trabeculectomy remains the standard procedure. Adjunctive treatment with subconjunctival
mitomycin or fluorouracil is used perioperatively or postoperatively in worse prognosis cases. A variety of less
invasive procedures that avoid a full-thickness incision into
the eye, called microinvasive glaucoma surgery, are appropriate for moderate glaucoma and are associated with
fewer complications but can be more difficult to perform.
2. Angle-closure glaucoma—In chronic angle-closure
glaucoma, laser peripheral iridotomy, surgical peripheral
iridectomy, or cataract extraction may be helpful. In patients
with asymptomatic narrow anterior chamber angles, which
includes about 10% of Chinese adults, prophylactic laser
peripheral iridotomy can be performed to reduce the risk of
acute and chronic angle-closure glaucoma. However, there
are concerns about the efficacy of such treatment and the
risk of cataract progression and corneal decompensation. In
the United States, about 1% of people over age 35 years have
narrow anterior chamber angles, but acute and chronic
angle closure are sufficiently uncommon that prophylactic
therapy is not generally advised.
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3. Normal-tension glaucoma—The goal of treatment for
normal-tension glaucoma is reduction in intraocular pressure by 30% (even if it is in the normal range) to prevent
progression. As with open-angle glaucoma, if intraocular
pressure is not lowered with medical therapy alone, laser
trabeculoplasty is used as an adjunct. Trabeculectomy is
the standard surgical procedure if medical and laser therapy are inadequate.
» Prognosis
Untreated chronic glaucoma that begins at age 40–45 years
will probably cause complete blindness by age 60–65. Early
diagnosis and treatment can preserve useful vision
throughout life. In primary open-angle glaucoma and if
treatment is required in ocular hypertension, the aim is to
reduce intraocular pressure to a level that will adequately
reduce progression of visual field loss. In eyes with marked
visual field or optic disk changes, intraocular pressure must
be reduced to less than 16 mm Hg. In normal-tension glaucoma with progressive visual field loss, it is necessary to
achieve even lower intraocular pressure such that surgery
is often required.
» When to Refer
All patients with suspected chronic glaucoma should be
referred to an ophthalmologist.
Gedde SJ et al. American Academy of Ophthalmology Preferred
Practice Pattern Glaucoma Panel. Primary Open-Angle
Glaucoma Preferred Practice Pattern®. Ophthalmology.
2021;128:71. [PMID: 34933745]
Gedde SJ et al. American Academy of Ophthalmology Preferred
Practice Pattern Glaucoma Panel. Primary Open-Angle
Glaucoma Suspect Preferred Practice Pattern®. Ophthalmology.
2021;128:151. [PMID: 34933743]
Kang JM et al. Glaucoma. Med Clin North Am. 2021;105:493.
[PMID: 33926643]
Stein JD et al. Glaucoma in adults—screening, diagnosis, and
management: a review. JAMA. 2021;325:164. [PMID:
33433580]
UVEITIS
and by which ocular anatomic locations are involved (anterior, intermediate, posterior, or all [panuveitis]).
In most cases the pathogenesis of uveitis is primarily
immunologic, but infection may be the cause, particularly
in immunodeficiency states.
1. Nongranulomatous anterior uveitis—The systemic
disorders associated with acute nongranulomatous anterior uveitis are the HLA-B27-related conditions (ankylosing spondylitis, reactive arthritis, psoriasis, ulcerative
colitis, and Crohn disease). The initial presentation of
Behçet syndrome, a chronic recurrent disease, is usually
acute anterior uveitis, with recurrent hypopyon, and posterior uveitis, characteristically with branch retinal vein
occlusions. Both herpes simplex and herpes zoster infections may cause acute nongranulomatous and granulomatous anterior uveitis as well as retinitis (acute retinal
necrosis). Chronic nongranulomatous anterior uveitis
occurs in juvenile idiopathic arthritis.
2. Granulomatous anterior uveitis—Diseases producing
granulomatous anterior uveitis also tend to be causes of
posterior uveitis. These include sarcoidosis, toxoplasmosis,
tuberculosis, syphilis, Vogt-Koyanagi-Harada disease
(bilateral uveitis associated with alopecia, poliosis [depigmented eyelashes, eyebrows, or hair], vitiligo, and hearing
loss), and sympathetic ophthalmia that occurs after penetrating ocular trauma. In toxoplasmosis, there may be evidence of previous episodes of retinochoroiditis. Syphilis
characteristically produces a “salt and pepper” fundus but
may present with a wide variety of clinical manifestations.
The principal pathogens responsible for ocular inflammation in HIV infection are cytomegalovirus (CMV), herpes
simplex and herpes zoster viruses, mycobacteria, Crypto-
coccus, Toxoplasma, and Candida.
Retinal vasculitis and intermediate uveitis predominantly manifest as posterior uveitis with central or peripheral retinal abnormalities in retinal vasculitis and far
peripheral retinal abnormalities (pars planitis) in intermediate uveitis. Retinal vasculitis can be caused by a wide
variety of infectious agents and noninfectious systemic
conditions but also may be idiopathic. Intermediate uveitis
is often idiopathic but can be due to multiple sclerosis or
sarcoidosis.
ESSENTIALS OF DIAGNOSIS
»
Usually immunologic but possibly infectious or
neoplastic.
»
Inflammation may be confined to the eye or may
be systemic.
»
Acute anterior uveitis: sudden redness and blurry
vision often with photophobia.
»
Posterior uveitis: gradual loss of vision, commonly
with floaters, in a variably inflamed eye.
» General Considerations
Intraocular inflammation (uveitis) is clinically classified as
acute or chronic, as nongranulomatous or granulomatous,
» Clinical Findings
Anterior uveitis is characterized by inflammatory cells and
flare, best visualized with a slit lamp within the aqueous
humor. In severe cases, there may be hypopyon (layered collection of white cells) and fibrin within the anterior chamber. Cells may also be seen on the corneal endothelium as
keratic precipitates. In granulomatous uveitis, there are large
“mutton-fat” keratic precipitates, and sometimes iris nodules. In nongranulomatous uveitis, the keratic precipitates
are smaller or absent with no iris nodules. The pupil is usually small, and with the development of posterior synechiae
(adhesions between the iris and anterior lens capsule), it also
becomes irregularly shaped and poorly reactive.
Nongranulomatous anterior uveitis tends to present
acutely with unilateral pain, redness, photophobia, and
visual loss. However, the ocular inflammation associated
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with juvenile idiopathic arthritis is frequently indolent,
commonly asymptomatic initially, and carries a high
risk of sight-threatening complications. Granulomatous
anterior uveitis is also frequently chronic, recurrent, and
indolent, causing blurred vision in a variably inflamed
eye.
In posterior uveitis, there are cells in the vitreous and
there may be inflammatory retinal or choroidal lesions.
New retinal lesions are yellow with indistinct margins and
there may be retinal hemorrhages. Older lesions have more
defined margins and are commonly pigmented. Retinal
vessel sheathing may occur adjacent to such lesions or
more diffusely. In severe cases, vitreous opacity precludes
visualization of retinal details.
Posterior uveitis can be unilateral or bilateral with
symptoms of floaters and visual loss. Symptoms are commonly slower in onset, though acute presentations can
occur. Visual loss may be due to vitreous haze and opacities, inflammatory lesions involving the macula, macular
edema, retinal vein occlusion, or rarely, optic
neuropathy.
» Differential Diagnosis
Retinal detachment, intraocular tumors, and CNS lymphoma may all masquerade as uveitis.
» Treatment
Anterior uveitis usually responds to topical corticosteroids
(Table 7–2). Occasionally, periocular or intraocular corticosteroid injections or even systemic corticosteroids are
required. Dilation of the pupil with a cycloplegic agent (eg,
cyclopentolate, homatropine, atropine) (Table 7–2) is
important to relieve discomfort and prevent permanent
posterior synechiae. Posterior uveitis more commonly
requires systemic, periocular, or intravitreal corticosteroid
therapy. In chronic cases, systemic corticosteroid-sparing
immunomodulatory therapy with agents such as azathioprine, cyclosporine, mycophenolate, methotrexate, tacrolimus, or sirolimus is commonly required. Biologic therapies
are also often used. Pupillary dilation is not usually
necessary.
If an infectious cause is identified, specific antimicrobial therapy is often needed. In general, the prognosis for
anterior uveitis, particularly the nongranulomatous type, is
better than for posterior uveitis.
» When to Refer
• Any patient with suspected acute uveitis should be
referred urgently to an ophthalmologist or emergently
if there is visual loss or severe pain.
• Any patient with suspected chronic uveitis should be
referred to an ophthalmologist, urgently if there is more
than mild visual loss.
» When to Admit
Patients with severe uveitis, particularly those requiring
intravenous therapy, may require hospital admission.
Al-Janabi A et al. Long-term outcomes of treatment with bio-
logical agents in eyes with refractory, active, noninfectious
intermediate uveitis, posterior uveitis, or panuveitis. Ophthalmology. 2020;127:410. [PMID: 31607412]
Rathinam SR et al; FAST Research Group. Effect of
corticosteroid-sparing treatment with mycophenolate
mofetil vs methotrexate on inflammation in patients with
uveitis: a randomized clinical trial. JAMA. 2019;322:936.
[PMID: 31503307]
CATAR AC T
ESSENTIALS OF DIAGNOSIS
»
Gradually progressive blurred vision.
»
No pain or redness.
»
Lens opacities (may be grossly visible).
» General Considerations
Cataracts are opacities of the crystalline lens and are usually bilateral. They are the leading cause of blindness
worldwide. Age-related cataract is by far the most common
cause. Other causes include (1) congenital (from intrauterine infections, such as rubella and CMV, or inborn errors
of metabolism, such as galactosemia); (2) traumatic; (3)
secondary to systemic disease (diabetes mellitus, myotonic
dystrophy, atopic dermatitis); (4) topical, systemic, or
inhaled corticosteroid treatment; (5) uveitis; or (6) radiation exposure. Most persons over age 60 have some degree
of lens opacity. Cigarette smoking increases the risk of cataract formation. Multivitamin/mineral supplements and
high dietary antioxidants may prevent the development of
age-related cataract.
» Clinical Findings
The predominant symptom is progressive blurring of
vision. Glare, especially in bright light or with night driving; change of focusing, particularly development of
nearsightedness; and monocular double vision may
occur.
Even in its early stages, a cataract can be seen through a
dilated pupil with an ophthalmoscope or slit lamp. As the
cataract matures, the retina will become increasingly difficult to visualize, until finally the fundus reflection is absent
and the pupil is white.
» Treatment
Functional visual impairment, specifically its effect on
daily activities and increased risk of falls, is the prime criterion for surgery. The cataract is usually removed by one
of the techniques in which the posterior lens capsule
remains (extracapsular), thus providing support for a prosthetic intraocular lens. Ultrasonic fragmentation (phacoemulsification) of the lens nucleus and foldable intraocular
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lenses allow cataract surgery to be performed through a
small incision without the need for sutures, thus reducing
the postoperative complication rate and accelerating visual
rehabilitation. The standard monofocal prosthetic intraocular lens can correct near or far vision. Premium intraocular lenses (multifocal, extended depth of focus, and
accommodative) reduce the need for both distance and
near vision correction. In the developing world, manual
small-incision surgery, in which the lens nucleus is
removed intact, is popular because less equipment is
required. Additional laser treatment may be required subsequently (months to years after the initial cataract surgery) if the posterior capsule opacifies. The use of topical
eye drops to dissolve or prevent cataracts has shown promising results in experimental models; surgery, however, is
currently the only treatment option for a visually significant cataract.
» Prognosis
Cataract surgery is cost-effective in improving survival and
quality of life. In the developed world, it improves visual
acuity in 95% of cases. In the other 5%, there is preexisting
retinal damage or operative or postoperative complications. In less developed areas, the improvement in visual
acuity is not as high, in part due to uncorrected refractive
error postoperatively. Nasolacrimal duct obstruction
increases the risk of intraocular infection (endophthalmitis). A large number of drugs, such as alpha-adrenoreceptor antagonists for benign prostatic hyperplasia or systemic
hypertension and antipsychotics, increase the risk of complications during surgery (floppy iris syndrome) and in the
early postoperative period.
The alpha-blocker tamsulosin has the greatest risk of
floppy iris syndrome. There is no consensus about whether
to stop alpha-blockers before surgery because the effects of
the drug on the iris can persist for months to years. The
surgeon must know if the patient is taking an alpha-blocker
to prepare for iris issues during surgery. If the patient has
not yet started an alpha-blocker and is planning to have
cataract surgery shortly, it is best to wait until after surgery
to begin the medication, if possible.
» When to Refer
Patients with cataracts should be referred to an ophthalmologist when their visual impairment adversely affects
their everyday activities.
RETINAL DETACHMENT
ESSENTIALS OF DIAGNOSIS
»
Loss of vision in one eye that is usually rapid, possibly with “curtain” spreading across field of vision.
»
No pain or redness.
»
Detachment seen by ophthalmoscopy.
» General Considerations
Most cases of retinal detachment are due to development of
one or more peripheral retinal tears or holes (rhegmatogenous retinal detachment). This usually results from posterior vitreous detachment, related to degenerative changes
in the vitreous, and often occurs in persons over 50 years of
age. Nearsightedness and cataract extraction are the two
most common predisposing causes. It may also be caused
by penetrating or blunt ocular trauma, sometimes years
earlier.
Tractional retinal detachment occurs when there is
preretinal fibrosis, such as in proliferative retinopathy due
to diabetic retinopathy or retinal vein occlusion, or as a
complication of rhegmatogenous retinal detachment. Exudative retinal detachment results from accumulation of
subretinal fluid, such as in neovascular age-related macular
degeneration or secondary to choroidal tumor.
» Clinical Findings
Rhegmatogenous retinal detachment usually starts in the
peripheral retina, spreading rapidly to cause visual field
loss. Symptoms of the predisposing posterior vitreous
detachment with vitreoretinal traction include recent onset
of or increase in floaters (moving spots or strands like cobwebs in the visual field) and photopsias (flashes of light).
Central vision remains intact until the central macula
becomes detached. On ophthalmoscopic examination, the
retina may be seen elevated in the vitreous cavity with an
irregular surface (Figure 7–1). In tractional retinal detachment, there is irregular retinal elevation adherent to scar
tissue on the retinal surface, sometimes extending into the
vitreous. Exudative retinal detachments are dome-shaped
and the subretinal fluid shifts position with changes in
posture. Ocular ultrasonography assists the detection and
characterization of retinal detachment.
Christou CD et al. Intraoperative floppy iris syndrome: updated
perspectives. Clin Ophthalmol. 2020;14:463. [PMID:
32109982]
Lian RR et al. The quest for homeopathic and nonsurgical cata-
ract treatment. Curr Opin Ophthalmol. 2020;31:61. [PMID:
31770163]
Miller KM et al. American Academy of Ophthalmology Pre-
ferred Practice Pattern Cataract/Anterior Segment Panel.
Cataract in the Adult Eye Preferred Practice Pattern®. Ophthalmology. 2022;129:1. [PMID: 34780842]
» Treatment
Treatment of rhegmatogenous retinal detachments requires
closing all the retinal tears and holes by forming a permanent adhesion with laser photocoagulation to the retina or
cryotherapy to the sclera. Certain types of uncomplicated
retinal detachment may be treated by pneumatic retinopexy, in which an expansile gas is injected into the vitreous
cavity and the patient’s head is positioned to facilitate
apposition between the gas and the hole, which permits
DISORDERS OF THE EYES & LIDS
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▲
Figure 7–1. Inferior retinal detachment as seen on
direct or indirect ophthalmoscopy.
reattachment of the retina. Once the retina is reattached,
the retinal defects are surrounded by laser photocoagulation or cryotherapy scars; these two methods are also used
to seal retinal defects without associated detachment.
In complicated retinal detachments, particularly tractional retinal detachments, retinal reattachment can be
accomplished only by vitrectomy, direct manipulation of
the retina, and internal tamponade of the retina with air,
expansile gas, or silicone oil. The presence of an expansile
gas within the eye is a contraindication to air travel, mountaineering at high altitude, and nitrous oxide anesthesia, all
of which can cause the gas to expand with severe increases
in intraocular pressure. Such gases persist in the globe for
weeks after surgery (see Chapter 39). Treatment of exudative retinal detachments is determined by the underlying
cause.
» Prognosis
About 90% of uncomplicated rhegmatogenous retinal
detachments can be cured with one operation. The visual
prognosis is worse if the macula is detached or if the
detachment is of long duration.
CMDT 2025
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minimize eye motion; in some patients, patching both eyes
can be helpful in preventing the eyes from moving until
surgery can be performed to repair the retinal
detachment.
Sena DF et al. Pneumatic retinopexy versus scleral buckle for
repairing simple rhegmatogenous retinal detachments.
Cochrane Database Syst Rev 2021;11:CD008350. [PMID:
34762741]
Starr MR et al. Primary retinal detachment outcomes study:
summary of reports number 1 to number 18. Curr Opin Ophthalmol 2023;34:211. [PMID: 36866845]
VITREOUS HEMORRHAGE
Patients with vitreous hemorrhage complain of sudden
visual loss, abrupt onset of floaters that may progressively
increase in severity, or occasionally, “bleeding within the
eye.” Visual acuity ranges from 20/20 (6/6) to light perception. The eye is not inflamed, red, or painful, and clues to
diagnosis are inability to see fundus details or localized
blood in the vitreous, in front of the retina. Causes of vitreous hemorrhage include retinal tear (with or without
detachment), diabetic or sickle cell retinopathy, retinal
vein occlusion, retinal vasculitis, neovascular age-related
macular degeneration, retinal arterial macroaneurysm,
blood dyscrasia, therapeutic anticoagulation, trauma, subarachnoid hemorrhage, and severe straining (Valsalva
retinopathy).
» When to Refer
All patients with suspected vitreous hemorrhage must be
referred urgently to an ophthalmologist to determine the
etiology. If the vitreous hemorrhage is caused by a retinal
tear or detachment, it must be repaired urgently to prevent
permanent vision loss.
Fallico M et al. Intravitreal anti-vascular endothelial growth fac-
tors, panretinal photocoagulation and combined treatment for
proliferative diabetic retinopathy: a systematic review and
network meta-analysis. Acta Ophthalmol 2021;99:e795.
[PMID: 33326183]
Shaikh N et al. Vitreous hemorrhage–causes, diagnosis, and man-
agement. Indian J Ophthalmol 2023;71:28. [PMID: 36588205]
» When to Refer
All cases of retinal detachment must be referred urgently to
an ophthalmologist, and emergently if central vision is
good because this indicates that the macula has not yet
detached. During transportation, the patient’s head is positioned so that the retinal tear is placed at the lowest point
of the eye to minimize extension of the detached retina. If
the inferior retina is detached with superior visual field
loss, the patient should keep the head upright so that the
tear is located at the lowest point, whereas if the temporal
retina is detached (visual field loss on the side by the nose),
the patient should keep the temporal side of the head (ear
side) down to reduce the chances that the fluid will extend
beneath the central retina, causing the macula to detach. If
vision is good and the macula is attached, patients should
AGERELATED MACULAR DEGENERATION
ESSENTIALS OF DIAGNOSIS
»
Older age group.
»
In one or both eyes; acute or chronic deterioration
of central vision; distortion or abnormal size of
images, sometimes developing acutely.
»
No pain or redness.
»
Classified as dry (“atrophic,” “geographic”) or wet
(“neovascular,” “exudative”) macular degeneration.
»
Macular abnormalities seen by ophthalmoscopy.
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» General Considerations
Age-related macular degeneration is the leading cause of
permanent visual loss in the older population. Its prevalence progressively increases over age 50 years (to almost
30% by age 75). Its occurrence and response to treatment
are likely influenced by genetically determined variations,
many of which involve the complement pathway. Other
associated factors are sex (slight female predominance),
family history, hypertension, hypercholesterolemia, CVD,
farsightedness, light iris color, and cigarette smoking (the
most readily modifiable risk factor).
Although both dry and wet age-related macular degeneration are progressive and usually bilateral, they differ in
manifestations, prognosis, and management.
» Clinical Findings
Drusen are the hallmark of age-related macular degeneration. Hard drusen appear as discrete yellow subretinal
deposits. Soft drusen are paler and less distinct. Large,
confluent soft drusen are risk factors for neovascular (wet)
age-related macular degeneration. Vision loss in agerelated macular degeneration involves the central vision
only in most patients. Peripheral fields, and hence navigational vision, are maintained, except in patients with severe
neovascular age-related macular degeneration or in
patients with coincident optic nerve disease such as glaucoma. Although “dry” age-related macular degeneration is
more common, untreated “wet” age-related macular
degeneration accounts for about 90% of all cases of legal
blindness due to age-related macular degeneration.
1. “Dry” age-related macular degeneration—There is
gradual progressive bilateral visual loss due to geographic
atrophy of the outer retina, the retinal pigment epithelium,
and the choriocapillaris, which supplies blood to both the
outer retina and the retinal pigment epithelium.
2. “Wet” age-related macular degeneration—Choroidal
new vessels grow under either the retina or the retinal pigment epithelial cells, leading to accumulation of exudative
fluid, hemorrhage, and fibrosis. The onset of visual loss is
more rapid and more severe than in atrophic degeneration.
The two eyes are frequently affected sequentially over a
period of a few years.
mildly increased risk of choroidal neovascularization, and
intravitreal injection is associated with risks of infection
(1/2000), retinal detachment (1/10,000), vitreous hemorrhage, and cataract. As with wet degeneration, rehabilitation including low-vision aids is important. In addition,
patients should be advised to stop smoking cigarettes and
to take vitamin supplements as described above.
2. “Wet” age-related macular degeneration—Inhibitors of
vascular endothelial growth factors (VEGF), such as
ranibizumab, bevacizumab, aflibercept, faricimab, and
brolucizumab, and biosimilar medications, such as ranibizumab-nuna and ranibizumab-eqrn, can cause regression of
choroidal neovascularization with resorption of subretinal
fluid and improvement or stabilization of vision. Long-term
repeated intraocular injections are required and must be
administered in the eye clinic several times a year, if not
monthly. Treatment is well tolerated with minimal adverse
effects, but there is a risk of infection, retinal detachment, vitreous hemorrhage, and cataract. Brolucizumab has been associated with intraocular inflammation and occlusive retinal
vasculitis resulting in irreversible vision loss in some patients.
Some patients do not respond to anti-VEGF injections, and up
to one-third of eyes lose vision despite regular treatment.
» When to Refer
Older patients with sudden visual loss, particularly paracentral or central distortion or scotoma with preserved
central acuity, should be referred urgently to an
ophthalmologist.
Cabral de Guimaraes TA et al. Treatments for dry age-related
macular degeneration: therapeutic avenues, clinical trials and
future directions. Br J Ophthalmol. 2022;106:297. [PMID:
33741584]
Koh GY et al. Viewpoints: dual-blocking antibody against
VEGF-A and angiopoietin-2 for treating vascular diseases of
the eye. Trends Mol Med. 2022;28:347. [PMID: 35396185]
Tzoumas N et al. Complement inhibitors for age-related macular
degeneration. Cochrane Database Syst Rev. 2023;6:CD009300.
[PMID: 37314061]
CENTRAL & BRANCH RETINAL
VEIN OCCLUSIONS
» Treatment
No dietary modification has been shown to prevent the development of age-related macular degeneration, but its progression may be reduced by oral treatment with antioxidants
(vitamins C and E), zinc, copper, and carotenoids (lutein and
zeaxanthin, rather than vitamin A [beta-carotene]). Oral
omega-3 fatty acids do not provide additional benefit.
1. Dry age-related macular degeneration—Pegcetacoplan
and avacincaptad pegol are agents approved by the US
Food and Drug Administration (FDA) for treatment of this
disorder. Both agents inhibit the complement pathway, are
delivered by monthly or every-other-monthly injection
into the vitreous, and slow the rate of growth of geographic
atrophy lesions. However, both agents are associated with
ESSENTIALS OF DIAGNOSIS
»
Sudden monocular loss of vision.
»
No pain or redness.
»
Widespread or sectoral retinal hemorrhages.
» General Considerations
Central and branch retinal vein occlusion are common
causes of acute vision loss, with branch vein occlusions
being four times more common. The major predisposing
factors are the etiologic factors associated with arteriosclerosis, but glaucoma is also a major risk factor.
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» Clinical Findings
A. Symptoms and Signs
1. Central retinal vein occlusion—Ophthalmoscopic
signs include widespread retinal hemorrhages, retinal
venous dilation and tortuosity, retinal cotton-wool spots,
and optic disk swelling. Rarely, central retinal vein occlusion presents with severe vision loss and pain when neovascularization of the iris develops, usually about 90 days
after a central retinal vein occlusion has caused severe retinal nonperfusion.
2. Branch retinal vein occlusion—Sudden loss of vision
may occur at the time of occlusion if the fovea is involved,
or some time afterward from vitreous hemorrhage due to
retinal new vessels. More gradual visual loss may occur
with development of macular edema. In acute branch retinal vein occlusion, the retinal abnormalities (hemorrhages,
microaneurysms, venous dilation and tortuosity, and
cotton-wool spots) are confined to the area drained by the
obstructed vein.
To assess for possible reversible risk factors, check
blood pressure and ask about tobacco smoking in all
patients, and ask women about estrogen therapy (including
combined oral contraceptives). Patients should be asked
about a history of glaucoma and should undergo a comprehensive eye examination to check intraocular pressure.
A sleep study to assess for obstructive sleep apnea may be
recommended.
B. Laboratory Findings
Obtain screening laboratory studies for diabetes mellitus,
hyperlipidemia, and hyperviscosity (especially in simultaneous bilateral disease), including serum protein electrophoresis for paraproteinemia. Particularly in younger
patients, consider obtaining antiphospholipid antibodies,
lupus anticoagulant, tests for inherited thrombophilia, and
plasma homocysteine levels.
B. Neovascularization
Eyes at risk for neovascular glaucoma following ischemic
central retinal vein occlusion should be treated with panretinal laser photocoagulation prophylactically or as soon
as there is evidence of neovascularization, with the latter
approach necessitating frequent monitoring. Regression of
retinal and iris neovascularization can be achieved with
intravitreal injections of bevacizumab or other anti-VEGF
agents, but panretinal laser photocoagulation is the definitive treatment and cannot be substituted by anti-VEGF
agents. In branch retinal vein occlusion complicated by
retinal neovascularization, the ischemic retina should be
treated with laser photocoagulation.
» Prognosis
In central retinal vein occlusion, severity of visual loss initially is a good guide to visual outcome. Initial visual acuity
of 20/60 (6/18) or better indicates a good prognosis. Visual
prognosis is poor for eyes with neovascular glaucoma. In
branch retinal vein occlusion, visual outcome is determined by the severity of glaucoma and macular damage
from hemorrhage, ischemia, or edema.
» When to Refer
All patients with retinal vein occlusion should be referred
urgently to an ophthalmologist.
Kapur M et al. Future of anti-VEGF: biosimilars and biobetters.
Int J Retina Vitreous. 2022;8:2. [PMID: 34983660]
Romano F et al. Update on retinal vein occlusion. Asia Pac J
Ophthalmol (Phila). 2023;12:196. [PMID: 36912792]
CENTRAL & BRANCH RETINAL
ARTERY OCCLUSIONS
ESSENTIALS OF DIAGNOSIS
» Complications
If central retinal vein occlusion is associated with widespread retinal ischemia, manifesting as poor visual acuity (20/200 [6/60] or worse), florid retinal hemorrhages,
an afferent pupillary defect, and extensive areas of capillary closure on fluorescein angiography, there is a high
risk of development of neovascular (rubeotic) glaucoma,
typically within the first 3 months after the occlusion.
Branch retinal vein occlusion may be complicated by
peripheral retinal neovascularization or chronic macular edema.
» Treatment
A. Macular Edema
Intravitreal injection of VEGF inhibitors, including
ranibizumab, bevacizumab, or aflibercept and biosimilar
medications, is beneficial in patients with macular edema
due to either branch or central retinal vein occlusion.
»
Sudden monocular loss of vision.
»
No pain or redness.
»
Widespread or sectoral pale retinal swelling.
» General Considerations
Acute retinal arterial ischemia, including central and
branch retinal artery occlusion, is a true ocular and medical
emergency. In patients 50 years of age or older with central
retinal artery occlusion, giant cell arteritis must be considered (see Ischemic Optic Neuropathy and Chapter 22).
Otherwise, even if no retinal emboli are identified on ophthalmoscopy, urgent investigation for carotid and cardiac
sources of emboli must be undertaken in central and
branch retinal artery occlusion so that timely treatment can
be given to reduce the risk of stroke (see Chapters 14, 16,
and 26). Diabetes mellitus, hyperlipidemia, and systemic
hypertension are common etiologic factors. Migraine, oral
contraceptives, systemic vasculitis, congenital or acquired
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CHAPTER 7
thrombophilia, and hyperhomocysteinemia are also causes,
particularly in young patients. Internal carotid artery dissection should be considered, especially when there is neck
pain or a recent history of neck trauma.
» Clinical Findings
A. Symptoms and Signs
1. Central retinal artery occlusion—This occlusion pres-
ents as sudden profound monocular visual loss. Visual
acuity is usually reduced to counting fingers or worse,
and visual field may be restricted to an island of vision in
the temporal field. Ophthalmoscopy reveals pale swelling
of the retina with a cherry-red spot at the fovea
(Figure 7–2). Occasionally, emboli are seen in the central
retinal artery or its branches. The retinal swelling subsides over a period of 4–6 weeks, leaving a pale optic disk
with thinning of the inner retina on optical coherence
tomography scans; these findings can help diagnose
unexplained vision loss if the patient is not examined
during the acute occlusive event.
2. Branch retinal artery occlusion—This occlusion may
also present with sudden loss of vision if the fovea is
involved, but more commonly, sudden loss of a discrete
area in the visual field in one eye is the presenting complaint. Fundus signs of retinal swelling and sometimes
adjacent cotton-wool spots are limited to the area of retina
supplied by the occluded artery.
The clinician should identify risk factors for cardiac
sources of emboli including arrhythmia, particularly atrial
fibrillation, and cardiac valvular disease, and check the
blood pressure. Nonocular clinical features of giant cell
arteritis are age 50 years or older, headache, scalp
▲
Figure 7–2. Acute central retinal artery occlusion
with cherry-red spot (arrow) seen at the fovea centered
in macular loss of retinal transparency, and preserved
retinal perfusion (arrowheads) adjacent to the optic disk
due to macular cilioretinal artery supply. (Reproduced,
with permission, from Riordan-Eva P, Augsburger JJ.
Vaughan & Asbury’s General Ophthalmology, 19th ed.
McGraw Hill, 2018.)
tenderness, jaw claudication, general malaise, weight loss,
symptoms of polymyalgia rheumatica, and tenderness,
thickening, or absence of pulse of the superficial temporal
arteries. Table 22–11 lists the clinical manifestations of
vasculitis.
B. Laboratory Findings
Giant cell arteritis should be considered in cases of central
retinal artery occlusion without visible emboli. ESR and
CRP are usually elevated in giant cell arteritis, but one or
both may be normal (see Chapter 22). Consider screening
for other types of vasculitis (see Table 22–10). Screen for
diabetes mellitus and hyperlipidemia in all patients. Particularly in younger patients, consider testing for antiphospholipid antibodies, lupus anticoagulant, inherited
thrombophilia, and elevated plasma homocysteine.
C. Imaging
A brain MRI with diffusion-weighted imaging sequences
should be obtained urgently to look for cerebral infarction,
which is present in up to 31% of patients with branch or
central retinal artery occlusion. Obtain duplex ultrasonography of the carotid arteries, ECG, echocardiography with
transesophageal studies to identify carotid and cardiac
sources of emboli, and CT or MR studies for internal
carotid artery dissection, if necessary.
» Treatment
Retinal artery occlusions are a true emergency and
require urgent referral to an emergency department, ideally with a stroke center, for imaging and clinical assessment to prevent subsequent stroke. If the patient is seen
within a few hours after onset, emergency treatment,
comprising laying the patient flat, ocular massage, high
concentrations of inhaled oxygen, intravenous acetazolamide, and anterior chamber paracentesis, may influence
the visual outcome. Early thrombolysis, particularly by
local intra-arterial injection but also intravenously, has
shown good results in central retinal artery occlusion not
due to giant cell arteritis. However, local intra-arterial
injection of thrombolytic agents has a high incidence of
adverse effects and may be difficult to accomplish quickly
enough after the occlusion develops to prevent permanent vision loss due to inner retinal ischemia, which nonhuman primate studies suggest occurs within 90 minutes
of occlusion.
In giant cell arteritis, there is risk of involvement of the
other eye without prompt treatment. Recommended initial
empiric treatment once giant cell arteritis is suspected is
intravenous methylprednisolone 1 g/day for 3 days. All
patients require subsequent long-term corticosteroid therapy; concomitant administration of long-term low-dose
aspirin therapy is controversial. Tocilizumab, a monoclonal
antibody against the receptor for interleukin-6, is also
approved to treat giant cell arteritis. (See Polymyalgia
Rheumatica & Giant Cell Arteritis, Chapter 22, for further
discussion of treatment.)
Patients with embolic retinal artery occlusion with
70–99% ipsilateral carotid artery stenosis, and possibly
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those with 50–69% stenosis, should be considered for
carotid endarterectomy or possibly angioplasty with
stenting to be performed within 2 weeks (see Chapters 14
and 26). Retinal embolization due to cardiac disease
such as atrial fibrillation or a hypercoagulable state usually requires anticoagulation. Cardiac valvular disease
and patent foramen ovale may require surgical
treatment.
» When to Refer
• Patients with retinal artery occlusions should be
referred immediately to an emergency department, ideally with a stroke center, to evaluate for stroke
manifestations.
• Patients with central retinal artery occlusion should be
referred emergently to an ophthalmologist.
• Patients with branch retinal artery occlusion should be
referred urgently.
• Patients with suspected giant cell arteritis should be
referred to a rheumatologist to guide management.
» When to Admit
Patients with visual loss due to giant cell arteritis may
require emergency admission for high-dose corticosteroid
therapy and close monitoring to ensure adequate
treatment.
Flaxel CJ et al. Retinal and Ophthalmic Artery Occlusions Pre-
ferred Practice Pattern®. Ophthalmology. 2020;127:P259.
[PMID: 31757501]
Mac Grory B et al; American Heart Association Stroke Council;
Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; and Council on Peripheral
Vascular Disease. Management of central retinal artery occlusion: a scientific statement from the American Heart Association. Stroke. 2021;52:e282. [PMID: 33677974]
Webb Z. Intravenous thrombolysis for central retinal artery
occlusion: a look at the literature for the emergency medicine
physician. Cureus. 2023;15:e41878. [PMID: 37457612]
TRANSIENT MONOCULAR VISUAL LOSS
lasting a few minutes and a similar curtain effect as the
episode passes (amaurosis fugax; also called “fleeting
blindness”). An embolus is rarely seen on ophthalmoscopy.
Other causes of transient, often recurrent, visual loss due to
ocular ischemia are giant cell arteritis, hypercoagulable
state (such as antiphospholipid syndrome), hyperviscosity,
and severe occlusive carotid disease. More transient visual
loss, lasting only a few seconds to 1 minute, usually recurrent, and affecting one or both eyes, occurs in patients with
optic disk swelling, such as in those with raised intracranial
pressure.
B. Diagnostic Studies
In most cases, clinical assessment and investigations are
much the same as for retinal artery occlusion with emphasis on urgent neuroimaging to assess for cerebral infarction, and identification of a source of emboli, since
patients with embolic transient vision loss are at increased
risk for stroke, MI, and other vascular events. Optic disk
swelling requires different investigations (see Optic Disk
Swelling, below).
» Treatment
All patients with possible embolic transient visual loss
should be treated immediately with oral aspirin (at least 81
mg daily), or another antiplatelet drug, until the cause has
been determined. Affected patients with 70–99% (and possibly those with 50–69%) ipsilateral carotid artery stenosis
should be considered for urgent carotid endarterectomy or
possibly angioplasty with stenting (see Chapters 14 and 26).
In all patients, vascular risk factors (eg, hypertension) need
to be controlled. Retinal embolization due to cardiac
arrhythmia, such as atrial fibrillation, or a hypercoagulable
state usually requires anticoagulation. Cardiac valvular
disease and patent foramen ovale may require surgical
treatment.
» When to Refer
In all cases of episodic visual loss, early ophthalmologic
consultation is advisable.
ESSENTIALS OF DIAGNOSIS
»
Sudden-onset, monocular loss of vision usually
lasting a few minutes with complete recovery.
» Clinical Findings
A. Symptoms and Signs
Transient monocular visual loss (“ocular transient ischemic
attack [TIA]”) is usually caused by a retinal embolus from
ipsilateral carotid disease or the heart. The visual loss is
characteristically described as a curtain passing vertically
across the visual field with complete monocular visual loss
» When to Admit
Referral to a stroke center or hospital admission is recommended in embolic transient visual loss if there have been
two or more episodes in the preceding week (“crescendo
TIA”) or the underlying cause is cardiac or a hypercoagulable state.
Bhatia K et al. Contemporary antiplatelet and anticoagulant
therapies for secondary stroke prevention: a narrative review
of current literature and guidelines. Curr Neurol Neurosci
Rep. 2023;23:235. [PMID: 37037980]
Mbonde AA et al. Current guidelines on management of amau-
rosis fugax and transient ischemic attacks. Asia Pac J Ophthalmol (Phila). 2022;11:168. [PMID: 35213421]
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RETINAL DISORDERS ASSOCIATED WITH
SYSTEMIC DISEASES
1. Diabetic Retinopathy
ESSENTIALS OF DIAGNOSIS
»
By 20 years after diagnosis of diabetes, 99% of
patients with type 1 diabetes and 60% of patients
with type 2 diabetes will have diabetic
retinopathy.
»
Nonproliferative diabetic retinopathy: can be mild,
moderate, or severe. Microvascular changes are
limited to the retina.
»
Proliferative diabetic retinopathy: new blood vessels grow on the surface of the retina, optic nerve,
or iris.
»
Diabetic macular edema: central retinal swelling;
can occur with any severity level of diabetic retinopathy; can reduce visual acuity if the foveal
center is involved.
» General Considerations
Diabetic retinopathy is present in about one-third of
patients in whom diabetes has been diagnosed, and about
one-third of those have sight-threatening disease. In the
United States, it affects about 4 million people; it is the
leading cause of vision loss worldwide among adults aged
25–74 years; and the number of affected individuals aged
65 years or older is increasing. Worldwide, there are
approximately 93 million people with diabetic retinopathy, including 28 million with vision-threatening disease.
Retinopathy increases in prevalence and severity with
increasing duration and poorer control of diabetes. In type
1 diabetes, retinopathy is not detectable for the first 5
years after diagnosis. In type 2 diabetes, about 20% of
patients have retinopathy at diagnosis, likely because they
had diabetes for many years before diagnosis. Macular
involvement is the most common cause of legal blindness
in type 2 diabetes.
There are two main categories of diabetic retinopathy:
nonproliferative and proliferative. Diabetic macular edema
can occur at any stage in both nonproliferative and proliferative retinopathy and is the most common reason for
ophthalmic diabetic treatment.
Nonproliferative retinopathy (previously known as
“background” retinopathy) is subclassified as mild, moderate, or severe. It represents the earliest stage of retinal
involvement by diabetes. During this stage, the retinal
capillaries leak proteins, lipids, or red cells into the retina.
When this process occurs in the macula and causes clinically significant macular edema, visual acuity is affected;
this is the most common cause of visual impairment in
patients with type 2 diabetes.
Proliferative retinopathy is less common than nonproliferative retinopathy but causes more severe visual loss.
It involves the growth of new vessels and fibrous tissue on
the surface of the retina, extending into the vitreous chamber. It is a consequence of severe capillary occlusion, which
causes retinal ischemia and release of VEGF; this, in turn,
stimulates new vessel growth with vision loss from preretinal hemorrhage, fibrosis, and retinal traction.
» Clinical Findings
Clinical assessment comprises visual acuity testing, stereoscopic examination of the retina, retinal imaging with optical coherence tomography, and sometimes fluorescein
angiography.
Nonproliferative retinopathy manifests as microaneurysms, retinal hemorrhages, venous beading, retinal
edema, and hard exudates. In mild nonproliferative diabetic retinopathy, there are mild retinal abnormalities
without visual loss. Reduction of vision is most commonly
due to diabetic macular edema, which may be focal or diffuse, but it can also be due to macular ischemia. Severe
nonproliferative retinopathy is defined as having any one
of the following: severe intraretinal hemorrhages and
microaneurysms in four quadrants, venous beading in two
or more quadrants, or intraretinal microvascular abnormalities in at least one quadrant.
Proliferative retinopathy is characterized by neovascularization, arising from either the optic disk or the retinal
vascular arcades. Prior to proliferation of new capillaries, a
preproliferative phase often occurs in which arteriolar
ischemia is manifest as cotton-wool spots (small infarcted
areas of retina). Vision is usually normal until macular
edema, vitreous hemorrhage, or retinal detachment occurs.
Proliferation into the vitreous of blood vessels, with associated fibrosis, may lead to vitreous hemorrhage and tractional retinal detachment.
Diabetic retinopathy may worsen after bariatric surgery
or in patients with long-standing hyperglycemia that is
rapidly brought under tight control, such as after receiving
an insulin pump. It is believed that capillary endothelial
cells retain “metabolic memory” of hyperglycemia and that
epigenetic changes persist for several months after the
hyperglycemia is corrected, sometimes causing retinopathy
progression after intensive glycemic control is initiated;
however, after the first 18–24 months, rates of progression
are significantly lower in patients treated with intensive
control compared to conventional regimens.
» Screening
Visual symptoms and visual acuity are poor guides to the
presence of diabetic retinopathy. Patients with diabetes
mellitus should undergo regular fundus photography,
which can be performed using telemedicine that may
involve computer detection software programs, or dilated
slit-lamp examination of the retina. Ultrawide-field fluorescein angiography can identify peripheral retinal vascular lesions that predict disease worsening in eyes with
nonproliferative diabetic retinopathy. Patients with type 1
diabetes mellitus should be screened 5 years after the diabetes is diagnosed. Patients with type 2 diabetes mellitus
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