Inflammation of the anterior uveal tract is called iritis or anterior uveitis; when the adjacent ciliary body is also

inflamed the process

is called iridocyclitis. Patients with iritis may present in a similar fashion to those with an active corneal process but there is no
foreign body sensation per se.
Patients with an
active corneal
process and iritis
will display an
aversive
response when
the penlight is

shined in the
affected and in
the uninvolved
eye.
The cardinal sign of iritis is ciliary flush: injection that gives the appearance of a red ring around the iris. Typically, there is no
discharge and only minimal tearing.

Retinal Detachment: Course, definitions, and pathophysiology Without treatment, most symptomatic retinal detachments
progress to involve the entire retina and lead to loss of vision. Retinal detachments are classified as "rhegmatogenous" if they
are the result of a full-thickness retinal hole or retinal tear and as "nonrhegmatogenous" otherwise.
Rhegmatogenous detachments are most common, and they are most commonly a consequence of posterior vitreous
detachment (PVD), a normal event in people between the ages of 50 and 75. In some patients, areas of adhesion during PVD
can pull on the retina and cause a tear. Rhegmatogenous detachments can also occur after ocular trauma, though this is a rare
occurrence.
Nonrhegmatogenous detachments can occur in patients with proliferative diabetic retinopathy, retinal neovascularization, or
inflammatory conditions and in other settings.
Risk factors and clinical presentation Risk factors for rhegmatogenous detachments include myopia, focal thinning of the
periphery of the retinal called lattice degeneration, and a family history of retina tears or detachments. Asymptomatic retinal
breaks do not typically progress to retinal detachment. Patients with a symptomatic PVD who develop a full-thickness retinal
tear are at high risk for retinal detachment. The most common symptom of PVD is an increasing number of floaters in one eye.
Flashes of light (photopsias) are also common during PVD; and if a small retinal vessel is torn, the patient may note a shower of
black spots (red blood cells) and/or a marked decrease in vision. Patients with retinal detachment (due to PVD or other
etiologies) will typically note a peripheral visual field defect. Ophthalmoscopy shows grey elevated retina.
Diagnosis and management Patients with symptoms of a PVD should be quickly examined by an ophthalmologist to exclude
a retinal tear or detachment. Patients with a new and progressive visual field defect suggestive of a retinal detachment require
urgent evaluation. In the absence of retinal breaks or tears or vitreous pigmented cells, most patients with PVD require no
specific treatment but should be re-examined by an ophthalmologist in one to three months. Patients with a retinal hole or tear
in the presence of a symptomatic PVD should generally be treated by an ophthalmologist with laser photocoagulation or
cryoretinopexy to prevent retinal detachment. Patients with a retinal detachment will generally be treated with one or more of
the following procedures: laser or cryoretinopexy, pneumatic retinopexy, scleral buckle, or vitrectomy. Patients with small
peripheral retinal detachments may be treated with barrier procedures, such as cryoretinopexy or laser photocoagulation. Some
patients with asymptomatic rhegmatogenous retinal detachments may be closely monitored without therapy or treated with
barrier procedures.
Optic glioma is a well-known complication of neurobromatosis, type 1. It occurs in 15% of patients with this disease, mostly in
children younger than 6 years of age. A history of slowly progressive unilateral visual loss and dyschromatopsia are
characteristic- Exophthalmos is sometimes present on physical examination. The optic disk may be normal, swollen, or atrophic.
In HIV patients, both HSV and VZV can cause severe, acute retinal necrosis associated with pain, keratitis, uveitis, and funduscopic ndings of
peripheral pale lesions and central retinal necrosis. ln contrast, CMV retinitis is painless, not usually associated with keratitis or conjunctivitis,
and characterized by funduscopic ndings of hemorrhages and uffy or granular lesions around the retinal vessels.

Treatment of CMV retinitis: For patients with immediately sight-threatening lesions, we recommend initial therapy with an immediate

intravitreal injection ofganciclovir or foscarnet plus systemic therapy for CMV rather than systemic therapy alone. Criteria for
sight-threatening lesions are lesions <1500 microns from the fovea or adjacent to the optic nerve head. If systemic therapy is
initiated within 24 hours of the initial intravitreal injection, subsequent injections are probably not necessary. For
patients without immediately sight-threatening CMV retinitis, we recommend systemic therapy rather than local therapy.
Oral valganciclovir is as effective as intravenous therapy and is therefore typically the preferred systemic therapy.

Otosclerosis involves an abnormal remodeling of the otic capsule thought to be a possible autoimmune process in genetically susceptible
individuals- The stapes footplate becomes xed to the oval window, resulting in loss of its piston action. This disorder is sometimes
referred to as otospongiosis as CT scan may show a lucent (as opposed to sclerotic) focus in the temporal bone near the oval window.
Treatment involves hearing amplication or surgical stapedectomy.
Urgent ophthalmologic consultation is indicated in patients with suspected Angle closure glaucoma. The gold standard for diagnosis is
gonioscopy, in which an ophthalmologist uses a specialized prismatic lens with a slit lamp to visualize the iridocorneal angle- Ocular (eg,
Schiotz) tonometry measures lOP and can provide additional information if needed or if ophthalmologic consultation is not immediately
available.
Age-related macular degeneration: Treatment and prevention: smokers be advised to immediately quit smoking, to prevent

progression. There is no evidence that people without AMD should take antioxidants to prevent or delay the onset of this
disease.
Dry AMD treatment
We suggest that patients with extensive intermediate size drusen, at least one large druse, or
noncentral geographic atrophy in one or both eyes be treated with daily oral supplements consistent
with the AREDS2 formulation (containing vitamin C 500 mg, vitamin E 400 IU, lutein 10 mg,
zeaxanthin 1 mg, zinc 80 mg [as zinc oxide], and copper 2 mg [as cupric oxide]) Alternatively,
patients who are not smokers or former smokers may use the standard AREDS formulation, which
contains beta-carotene rather than lutein or zeaxanthin.
Wet AMD treatment In patients with wet AMD in one eye, treatment with Antioxidant and zinc
supplements(same as above) may decrease progression to advanced AMD in the fellow eye.
Effective specific therapies for exudative or wet AMD are intravitreous injection of a VEGF
inhibitor(bevacizumab, ranibizumab) possibly thermal laser photocoagulation (in selected patients), and
photodynamic therapy.