Professional Documents
Culture Documents
Ophthalmology
for Medical Students
A Syllabus for the Clerkship in Ophthalmology
Cynthia S. Chiu, MD
Assistant Professor of Ophthalmology
Weill School of Medicine, Cornell University
New York Presbyterian Hospital
with contributions by: D. Jackson Coleman, MD, Kip L. Dolphin, MD, and Thomas C. Lee, MD
References:
1. http://isgwww.cs.uni-magdeburg.de/~stefans/lehre/sfu/eye.jpg
2. http://anatomy.iupui.edu/courses/histo_D502/D502f04/lecture.f04/Eyef04/ret.jpg
3. http://www.cid.ch/DAVID/Bon/Bon20.html
4. http://www.chb-genomics.org/research/engle/images/nl-lateye.gif
5. http://eyelearn.med.utoronto.ca/OcuAnatLecture/images/Ocu_Anat_58.jpg
6. http://www.fz-juelich.de/ibi/ibi-1/datapool/page/181/figure%205-500.jpg
Endophthalmitis
Infection within the globe can result from ocular injury
(penetrating trauma or intraocular surgery) or
hematogenous spread (sepsis). The common culprits are
bacteria (staph, strep, Bacillus, and P.acnes) as well as
ubiquitous fungi (yeasts from indwelling catheters). The
vitreous is a nutritive jelly, much like agar, and bacterial
seeding of the vitreous can quickly turn the eye into a selfcontained abscess. Patients report loss of vision, pain,
and redness. Treatment consists of vitreous culture and
injection of broad spectrum intraocular antibiotics. Severe
loss of vision may necessitate surgical removal of the
vitreous abscess. Recovery is variable and depends on
the virulence of the organism.
Eyelid and Corneal Burns
Both thermal and chemical burns cause devastating injury
to the eyes. Early after injury, the eyelid skin can slough
and the tissue becomes edematous from fluid thirdspacing. As it heals, the skin contracts, and lid malpositioning causes corneal exposure and thinning.
Corneal and conjunctival defects also occur, and if limbal
stem cells are damaged, these evolve into non-healing
ulcers. Injury to the blood supply can cause ocular
ischemia. Of chemical burns, alkaline agents cause more
widespread damage due to deeper tissue penetration.
Patients with chemical burns must undergo irrigation until
the pH is neutralized. Aggressive lubrication and antibiotic
prophylaxis are standard treatment. With severe
inflammation, topical steroids can be used to minimize
long-term scarring and contraction.
Orbital Cellulitis
Infection of the orbit and periorbital tissues may extend
from adjacent sinusitis or be inoculated by skin trauma.
The pathogens most commonly implicated are staph,
strep, and H.flu. It is important to differentiate between
orbital and preseptal cellulitis; the former threatens the
orbital apex, the cavernous sinus, and the CNS; the latter
is limited to the skin. The orbital septum, a fibrous
membrane which extends from periosteum to the eyelids,
is the barrier which separates skin from deeper orbital
contents. Proptosis, limited motility, and decreased vision
are hallmarks of orbital involvement. Systemic antibiotics
are used to treat both, but orbital infection requires longterm therapy.
Orbital Fractures
Compressive forces during trauma can cause orbital blowout fractures. The bones which are thinnest and most
prone to fracture are the postero-medial floor (the
maxillary bone) and the medial wall (the lamina
papyrecea). Large fractures of the orbital floor will permit
the globe and orbital contents to sink inferiorly, resulting in
enophthalmos and diplopia. Small fractures may entrap
extraocular muscles, causing motility restriction, muscle
atrophy, and nausea/bradycardia (pulling on extraocular
muscles causes a vasovagal response). Fractures which
are functionally or cosmetically significant are repaired
using metal implants with antibiotic prophylaxis.
Conjunctivitis
Pink eye is the lay term for conjunctivitis, or inflammation
of the conjunctiva which is usually the transparent lining of
the globe. With inflammation, the conjunctiva becomes
edematous and the blood vessels become dilated. The
most common causes of conjunctivitis are viral, bacterial,
and allergic. The same viruses that cause the common
cold (adenovirus, enterovirus, etc) can also infect the eye,
causing teary/mucous discharge and irritation. Bacterial
infections are most often caused by strep, staph, and
H.flu, but may also be caused by gonococcus and
Chlamydia. The discharge is much thicker, more copious
and purulent. Patients with allergic disease complain of
itching and teary discharge. In all cases a history is
important for diagnosis. Bacterial infection is treated with
topical antibiotics (or systemic if gonococcal or
chlamydial). Allergic disease is treated with topical and
systemic antihistamines and mast cell stabilizers. There is
no treatment for viral conjunctivitis, but patients are given
contact precautions as it is highly contagious.
Blepharitis
Inflammation of the eyelids leads to chronic irritation,
foreign body sensation, and dryness. There are
specialized oil-secreting glands at the eyelid margins
which can become congested with lipid and infected with
skin flora. Shed skin cells, oil, and bacteria can
accumulate at the base of the lashes. Treatment for
blepharitis includes warm compresses, eyelid scrubs, and
artificial tears. Severe cases associated with rosacea
require systemic tetracyclines.
Chalazion
A stye, or hordeolum, is a small abscess that develops
within an eyelid oil gland. If it persists, a localized
granuloma, or chalazion, develops. Medical treatment
consists of warm compresses and antibiotic ointment, to
try to elicit the pus to the surface and induce spontaneous
drainage. If the chalazion fails to open on its own, surgical
curettage is necessary. Chalazia can be prevented if the
underlying condition, usually blepharitis, is well-controlled,
and therefore daily compresses and eyelid hygiene are
recommended.
Contact Dermatitis
An allergic dermatitis can develop from foreign soaps,
lotions, or makeup applied around the eye. The skin
becomes inflamed, with tissue edema, erythema, and
discomfort. The skin often has a corrugated appearance.
Differentiating from a preseptal cellulitis requires a careful
history, but often contact dermatitis extends over a wider
area (wherever the inciting substance was applied) and
the redness is more prominent. The offending agent
should be discontinued immediately. Often this alone is
enough. With more severe cases, a mild ophthalmic
steroid cream can be used to quiet the inflammation.
Cataract
Cataracts can be congenital or acquired. Simply put, a
cataract is the clouding of the crystalline lens, which
results in scattering, or diffraction, rather than focusing, or
refraction, of light. Congenital cataracts are caused by
insults to the fetus in utero. For senile cataracts, lens
fibers continue to add to the diameter of the lens over
time, much like the trunk of a tree. In addition, as patients
age, lens proteins become less soluble and precipitate,
causing the lens to change color and opacify. Symptoms
caused by cataract include blurred vision, difficulty with
reading, and glare. Treatment is by surgical removal, by a
process called phacoemulsification (highly concentrated
ultrasound with vacuum) and, in adults, replacement with
an artificial intraocular lens.
Glaucoma
Although the mechanism is not well understood, glaucoma
is a disease caused by elevated intraocular pressure or
vascular instability which causes damage to the optic
nerve. Acute glaucoma causes pain and rapid visual loss.
However, chronic glaucoma is often painless and patients
can lose a considerable number of optic nerve fibers, and
subsequently much peripheral vision, before they present.
The hallmark of glaucoma is a cupped nerve, where
nerve tissue is lost and consequently a large central crater
is formed (normally the central depression is less than 3040%). Visual field testing reveals loss of peripheral, and
sometimes central, vision. The goal of treatment is to
reduce the intraocular pressure, and this can be
accomplished with topical medications (aqueous
suppressants and outflow stimulants), laser treatment, and
filtering surgery.
Macular degeneration
Age-related macular degeneration (ARMD) is an idiopathic
disease that causes central visual loss in elderly patients.
In the dry form, a yellow substance called lipofuscin
deposits under the RPE in discrete lesions called drusen.
Drusen cause dysfunction and atrophy of the RPE. Since
the RPE is vital to the normal functioning of the retinal
photoreceptors and the blood-retinal barrier, visual loss
ensues. Dry ARMD is a slowly progressive disease with
no known cure. Recent studies have shown a diet rich in
anti-oxidant vitamins and smoking cessation can slow the
course of disease.
If there is enough damage to the RPE and the underlying
Bruchs membrane, choroidal vessels will break through
and gain access to the retina and subretinal space. This
choroidal neovascularization is comprised of abnormally
leaky capillaries which are fragile and prone to bleeding.
If this occurs, the disease transitions to the wet form of
macular degeneration. Macular hemorrhages can cause
instant and grave visual loss. Photodynamic therapy
(laser treatment combined with a drug which targets
abnormal choroidal vessels) can retard the progression of
disease but may not restore vision. Several new drugs
targeting stimulants to new vessel growth, namely VEGF,
are showing promising results.
Migraine
Migraines are thought to originate from vasospasm of the
cerebral arteries. In addition to debilitating headache,
nausea, photophobia, and phonophobia, migraines can be
accompanied by visual or other sensory auras. It is
important to recognize that the symptoms arise from the
visual cortex in the occipital lobe and not from the eyes.
Visual auras usually begin as scintillating scotomas,
shimmering curtains or colored geometric patterns. As the
migraine progresses, the positive visual phenomena can
expand to cover the visual field. In some patients,
negative phenomena can cause a hemianopia (or
blackout of half the visual field)! Treatment is aimed at
recognition of symptoms and serotonin agonists in
conjunction with neurological consultation.
Strabismus
In normal alignment of the eyes, the corneal light reflex is
centered in both pupils. Good alignment is necessary for
normal development of visual acuity and stereopsis, or
depth perception. Any misalignment results in competition
between the fovea of the two eyes (since the brain cannot
reconcile two different images both supposedly at the
center of vision). This causes one eye to develop a
central scotoma, or blind spot. Thus strabismus during
childhood results in amblyopia, or poor visual
development of one eye. Strabismus in adulthood (due to
trauma, thyroid disease, or sensory deprivation) can
cause diplopia and cosmetic concerns. In children,
patching for amblyopia (to strengthen the weaker eye)
should accompany surgical realignment. Adults who do
not opt for surgery can try prism glasses and patching.
References:
1. http://www.merck.com/media/mmhe2/figures/fg226_1.gif
2. http://www.cibavision.com/images/products/astigmatism.jpg
3. http://www.chall.com/Chall1/conjunctivitis_lg.gif
4. http://www.ueseyecare.com/images/photos/blepharitis_l.jpg
5. http://www.eyesearch.com/chalazion.jpg
6. http://www.allergycapital.com.au/Images/EyeDerm.jpeg
7. http://technology.kingston.ac.uk/dirc/medical/images/catara2.jpg
8. http://www.eyeatlas.com/box/96glaucoma_cupping.jpg
9. http://www.ohiovalleyeye.com/images/macdegen_K45_dry.jpg
10. http://macula.org/images/retina_wet.jpg
11. http://www.perret-optic.ch/optometrie/symptomes_diagnostiques/symptomes/symptomes_image/
opto_migraine_ophtalmic.gif
12. http://www.eyedr4kids.com/images/exotropia.jpg
Herpes Zoster
After chickenpox infection, the herpes zoster virus (HZV)
also remains dormant in the sensory ganglia.
Reactivation of HZV manifests as shingles, a painful
vesicular rash which, unlike HSV, strictly respects the
dermatomes. Virus latent in the trigeminal ganglion can
erupt in the V1 or V2 dermatomes, and can infect the eye.
Like HSV, HZV can cause conjunctivitis, corneal ulcers,
uveitis, and retinal necrosis. When the eye is involved,
topical and oral acyclovir limit viral replication while topical
steroids are used to treat the inflammation. Though HZV
does not recur in the eye, corneal scarring can cause
permanent visual loss. If this occurs, corneal transplant is
an option. Post-herpetic neuralgia is a chronic and
debilitating condition that is induced by sensory nerve
damage during the initial shingles outbreak, and can be
treated with neurontin or tricyclic antidepressants.
Uveitis
Inflammation within the eye has many etiologies. Any
cause of systemic inflammation (autoimmune disease,
infection, neoplasm) can also cause ocular disease.
Uveitis is characterized by pain, visual loss, glaucoma,
tissue necrosis, and scarring. Patients should undergo a
diagnostic work-up to evaluate for autoimmune and
infectious etiologies.
Uveitis can affect many different ocular tissues. Scleritis
is focal inflammation of the ocular wall, causing redness
and tenderness to touch. Iritis/iridocyclitis is inflammation
within the anterior chamber (white blood cells leaking from
the iris and ciliary body), and is commonly seen in juvenile
rheumatoid arthritis and HLA-B27 related diseases
(ankylosing spondylitis, Reiters, etc). Patients can
present with loss of vision, photophobia, and acute
glaucoma. With severe iritis, white blood cells can layer
into a precipitate called a hypopyon.
Posteriorly, retinitis, retinal vasculitis, and choroiditis can
occur in patients with systemic lupus erythematosus,
sarcoid, and various infectious organisms such as
tuberculosis, syphilis, and cytomegalovirus. Scarring and
necrosis here not only lead to visual loss but also to
secondary complications such as retinal detachment.
Optic neuritis, or inflammation along the optic nerve, is
often associated with multiple sclerosis. When the orbit,
extraocular muscles, and lacrimal gland are involved, the
term inflammatory orbital pseudotumor is used (to be
distinguished from pseudotumor cerebri).
Treatment of uveitis can be difficult with topical steroids
alone if the patient has concurrent systemic disease.
Though topical treatment is the first line of therapy for
intraocular disease, addition of systemic
immunosuppressives such as methotrexate, Cytoxan,
Imuran, and Embrel are often needed to keep the
inflammation under control. Patients are frequently comanaged with rheumatologists.
Retinopathy of Prematurity
Premature babies have underdeveloped lungs at birth and
are given supplemental oxygen therapy. However, their
retinas are also immature, and excess oxygen causes the
retinal vascular pattern to change. Neovascularization
occurs, with scaffolding of fibrovascular sheets into the
vitreous. Left untreated, these fibrovascular membranes
contract and cause retinal detachment. Premature babies
under 2000 grams must be monitored for the development
of retinopathy of prematurity (ROP). Once ROP begins,
treatment with laser or cryo (freezing) to the peripheral
retina is performed to induce regression of abnormal
vessels. These children must be monitored long-term for
the development of high myopia and strabismus that
accompany ROP.
Retinoblastoma
The most common malignant intraocular tumor of
childhood is retinoblastoma. The retinoblastoma gene
normally functions as a tumor suppressor. When one
allele is knocked out, either by a germline or somatic
mutation, damage to the second allele will result in the
formation of a white calcific tumor. Both eyes can be
affected, as can the pineal gland, which also contains
photoreceptor elements.
Affected children most commonly present with leukocoria
(white pupil) and strabismus. Small tumors confined to
the retina can be treated with laser and cryo. Large
tumors which threaten to metastasize can be treated with
chemo- and radio-therapy, or by enucleation (removal of
the eye). Siblings and parents should also be examined.
Unfortunately, patients with retinoblastoma often develop
other malignancies such as osteogenic sarcomas,
especially in the areas previously treated with radiation.
Papilledema
The strict definition of papilledema is elevated intracranial
pressure causing bilateral optic nerve edema. The causes
of papilledema include hydrocephalus, infection
(meningitis, encephalitis), space-occupying mass, and
idiopathic intracranial hypertension (pseudotumor cerebri).
Though visual acuity may not be affected initially, over
time papilledema can cause death of optic nerve fibers
and optic neuropathy and vision loss will result.
Treatment focuses on the inciting etiology. In cases of
idiopathic intracranial hypertension, intractable
papilledema can be treated by optic nerve fenestration, a
surgical procedure to create a window in the meninges
that line the optic nerve.
Optic Neuritis
Optic neuritis is the inflammation of the optic nerve. It can
be caused by many autoimmune, toxic, and infectious
processes, but it is commonly associated with multiple
sclerosis (MS). MS is an autoimmune disorder that
targets myelin, and is characterized by waxing and waning
neurological deficits and white matter lesions on MRI.
Optic neuritis presents with vision loss and pain with eye
movements. Often optic disc edema can be seen in the
affected eye. The natural course of disease is
spontaneous improvement, however patients with severe
vision loss can be treated with high-dose intravenous
steroids to accelerate recovery.
Stroke
Cerebral infarct along the visual pathways will cause
various patterns of visual loss, depending on the location
of injury. All lesions posterior to the optic chiasm will
cause bilateral visual field defects; the more posterior the
lesion, the more congruous the field defects will appear.
To determine the location of the stroke, the rule is as
follows: defects correspond to lesions in the opposite
hemisphere, and superior defects point to inferior lesions
(and vice versa). Optic tract lesions (C) can produce
homonymous hemianopias. Since fibers which serve the
superior visual field travel inferiorly to the temporal lobes
(D), lesions here create superior quadrantanopias or
segmental defects. Thus parietal lobe lesions produce
inferior defects. Occipital lobe lesions (E) can involve or
spare the center of vision, depending on the area
involved. Though little can be done to recover loss field,
visual rehabilitation and training can help patients cope
with their limited peripheral vision.
References:
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files/slide0036_image002.jpg
Glaucoma Surgery
Filtration surgery is performed when medications have
failed to reduce the intraocular pressure to a level that is
safe for the optic nerve. The goal of glaucoma surgery is
to create an alternative path by which intraocular fluid can
drain from the eye and be reabsorbed by the venous
circulation. The traditional trabeculectomy involves
creating a partial thickness flap in the sclera, which covers
a hole connecting the anterior chamber to the outside
world. The flap helps keep the efflux of fluid partially
controlled, so that hypotony does not develop. Aqueous
leaves the eye through the hole (sclerotomy), travels
under the flap and under the conjunctiva, to be
reabsorbed posteriorly by the ophthalmic veins. When the
scleral tissue is not healthy, artificial valves can be
implanted to act as a conduit for aqueous removal.
Strabismus Surgery
Realignment of the eyes can be done by mechanically
repositioning the extraocular muscles. Weak muscles are
shortened or moved forward to increase their actions.
Overactive muscles are shifted more posteriorly to cause
relaxation and weakening. Strabismus surgery is usually
performed on two muscles at a time, either corresponding
muscles on both eyes (both strengthened or weakened) or
antagonist muscles on the same eye (one strengthened
while the other weakened). In adult patients with complex
strabismus (such as thyroid disease), temporary knots can
be tied in the operating room, to be more finely adjusted in
the recovery room, with the patient awake and able to
cooperate.
Dacryocystorhinostomy
Chronic naso-lacrimal duct obstruction leads to excess
tearing and the potential for recurrent infection. To bypass
the blockage, a small opening in the nasal bone is made
adjacent to the lacrimal sac, and the mucosa of the sac
and the nasal cavity are joined. Then, silicone tubes are
passed through the lacrimal canaliculi, into the new
opening, and then retrieved from the nose and tied.
These tubes stay in place for several weeks while the new
passageway heals, to help maintain patency of the
openings, before they are removed.
Laser Surgery
There are numerous applications for laser
photocoagulation in ophthalmology. In refractive surgery,
laser energy is used to remodel the cornea and to change
its refractive power, to give patients clear vision without
the use of spectacles or contact lenses. In the anterior
segment, laser is used to perforate the iris (in acute angle
closure glaucoma), to remodel the drainage structures of
the eye (in chronic glaucoma), to open a clear window in
lens capsule opacities (behind an artificial lens), and to cut
buried sutures. In the posterior segment, laser is used to
treat proliferative retinopathies, including diabetic disease,
sickle cell disease, and ROP. By coagulating selected
sections of retina, there is decreased retinal metabolic
demand, and decreased production of the chemical
stimulants to neovascularization (such as VEGF). A new
form of laser is now the standard of care in macular
degeneration. Photodynamic therapy is the combination
of an intravenous drug which specifically targets abnormal
new vessels, followed by selective activation of the drug in
the eye through laser light. In orbital surgery, laser is also
used during dacryocystorhinostomy and in eyelid skin
resurfacing.
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