Ординатура / Офтальмология / Английские материалы / Manual for Eye Examination and Diagnosis_Leitman_2007

Symptoms include pain, blurred vision, halos, and nausea. Signs include a mid-dilated nonreactive pupil, corneal edema, and a reddened conjunctiva (Figs 231 and 232).

The pupil dilation precipitating this attack may be caused by catecholamine release associated with stress, or darkness, antihistamines, anticholinergics, sympathomimetics, and major tranquilizers.

Treatment of angle-closure glaucoma first requires lowering of the pressure. It may require oral Diamox and topical drops always including pilocarpine 1% so the pupil constricts. If the pressure still remains too high, a short acting hyperosmotic agent such as mannitol 20% i.v. or oral glycerine 50% may be administered. Both draw fluid out of the eye by increasing the osmolarity of the blood. Once the attack is arrested, the corneal edema clears so that a laser iridotomy can be performed (Fig. 233). This allows aqueous to flow into the anterior chamber and bypass the pupillary block. It is often a permanent cure.

Fig. 231 Acute angle-closure glaucoma with dilated pupil.

Fig. 232 Angle-closure glaucoma: shallow anterior chamber and corneal edema.

Less common types of glaucoma, called secondary open-angle glaucoma, could be caused by blockage of the trabecular meshwork by pigment (Fig. 234), hemorrhage, inflammatory cells (as in iritis), pseudoexfoliation (Fig. 235), or scarring from rubeosis iridis (Fig. 236).

The trabecular meshwork may be covered with a membrane in the case of infantile glaucoma.

Trauma could cause glaucoma by tearing the iris at its insertion on the ciliary body. Often, there is associated bleeding in the anterior chamber (Fig. 237) referred to as a hyphema. Complications of hyphema include rebleeds, associated retinal damage, and glaucoma. Rx: bilateral patch and absolute bedrest for 5 days.

Fig. 234 Pigmentary glaucoma.

Fig. 236 Rubeosis iridis. These abnormal iris blood vessels scar the angle of the eye. They most often result from ischemic retinal diseases such as proliferative diabetic retinopathy and central retinal artery or vein occlusion.

Fig. 233 Peripheral iridotomy at 2 o’clock.

Fig. 235 Pseudoexfoliation is identified by white flakes seen on the anterior lens capsule, pupillary margin, zonules, and trabecular meshwork. It is relatively common and is associated with an increased incidence of glaucoma and weakened zonules which could complicate cataract surgery.

Fig. 237 Hyphema with large iris disinsertion (dialysis) from its root.

Gonioscopy may reveal angle recession (Fig. 238) in which the iris insertion is shifted posteriorly, exposing a wide band of darkly pigmented ciliary body. Patients should be monitored indefinitely for glaucoma.

One type of juvenile glaucoma is Sturge– Weber syndrome (Fig. 239) in which there is also angiomatosis of the face and the meninges with cerebral calcifications and seizures.

Uvea (Figs 240 and 241)

The uvea is composed of the iris, ciliary body, and choroid. All three are contiguous, and contain pigmented melanocytes. The ciliary body is made up of the pars plicata and the pars plana (Figs 242 and 243). The pars plicata is anatomically the root of the iris. It

Fig. 238 Angle recessed posteriorly following traumatic hyphema. The recessed angle is seen as a wide dark band between the cornea and the iris.

Fig. 240 The uvea is made up of the iris, ciliary body, and choroid.

Fig. 242 Ciliary body.

Fig. 241 Uvea. Courtesy of Stephen

McCormick.

Fig. 243 Ciliary muscle focusing lens.

comprises ciliary processes that secrete aqueous, and the ciliary muscle, which focuses the lens by decreasing the tension on the zonules (Fig. 243). The pars plana is the flat structure connecting the pars plicata with the retina. Because it is relatively avascular, it can be used as the site to enter the eye in vitreous and retinal surgery.

Malignant melanoma

A melanocyte tumor is the most common primary intraocular malignancy. It is unilateral and develops from the choroid in 85% of cases, the ciliary body in 9%, and the iris in 6%. Choroidal lesions are elevated and usually slate gray, but may be white to black with yellow–gold and uneven pigmentation (Figs 244–246) unlike a benign nevus, which is usually a more uniform gray color and flat (Fig. 247). This must be distinguished from metastatic carcinoma to the eye, which is also most common in the choroid but is usually lighter in color. Most often the primary site is the breast or lung.

Sclera

Vitreous

Choroidal Melanoma

Fig. 246 B-scan ultrasound of a malignant choroidal melanoma showing typical domeshaped growth which helps to confirm the diagnosis. The scan also shows its size and whether it extends beyond the sclera which will determine the type of treatment. This eye, with this massive tumor, was enucleated.

Fig. 244 Malignant choroidal melanoma.

Fig. 245 Gross section of malignant melanoma treated with removal of eye (enucleation). An alternative treatment for smaller lesions is the placement of an episcleral radioactive plaque under the tumor or infrared laser treatment called “transpupillary thermal therapy.” The latter two may preserve vision.

Fig. 247 Benign choroidal nevus.

Benign iris freckles (Fig. 248) and nevi are common, whereas malignant iris melanoma (Figs 249 and 250) is extremely rare. Lesions become more suspicious if they are growing, elevated, vascularized, distort the pupil, or cause inflammation, glaucoma, or cataracts.

Rubeosis iridis is a serious condition in which abnormal vessels grow on the surface of the iris (Fig. 251) in response to ischemia associated with central retinal vein occlusion proliferative diabetic retinopathy, or carotid artery occlusive disease. Laser photocoagulation of the retina may cause regression of iris vessels. Untreated, the neovascularization causes a severe glaucoma.

An iris coloboma (Fig. 252) is due to failure of embryonic tissue to fuse inferiorly. It may also involve the choroid, lens, and optic nerve.

Anterior uveitis

This is an inflammation of the iris (iritis) and ciliary body (cyclitis). Cyclois a prefix referring to the ciliary body. It causes ocular pain, tearing, and photophobia. Signs include miosis (small pupil), perilimbal conjunctival injection (Fig. 253), and anterior chamber flare and cells (Fig. 254), Flare refers to the beam’s milky appearance due to elevated protein. With the slit lamp on high magnification and a short bright beam shining across the dark pupil, grade cells from barely visible (trace) to very many (4 ).

Fig. 248 Benign iris freckle.

Fig. 249 Malignant iris melanoma with elevated lesions and distorted pupil.

Fig. 250 Gonioscopic view of elevated iris melanoma. Courtesy of Michael P. Kelly.

Keratitic precipitates are deposits of inflammatory cells and protein on the corneal endothelium (Figs 255 and 257). Cyclitis typically reduces eye pressure, since the ciliary body secretes the aqueous, but in severe iritis eye pressure may become elevated if cellular debris obstructs the trabecular meshwork.

Another complication of uveitis is posterior synechiae. These are adhesions between the iris and the lens capsule (Fig. 255). To prevent this, the pupil is kept dilated and steroids are given to prevent a fibrinous sticky aqueous.

Treatment for iritis includes a topical cycloplegic such as cyclogel 1% and a steroid such as Pred Forte 1%. Frequency and strength of medication depends on the severity of the condition. Besides dilating the pupil, the cycloplegic also relieves the pain due to ciliary spasm.

This same action prevents accommodation of the lens, making this drug also useful in refracting children. Shorter acting anticholinergics are also used to dilate the pupil prior to retinal examination.

Iritis or cyclitis is caused most often by intraocular surgery, blunt ocular trauma, and corneal ulcers, abrasions, and foreign bodies. Next in frequency of causation is the finding of human leucocytic antigen 27 (HLA-27) on blood tissue typing. It occurs in about 25% of patients with anterior uveitis and no associated disease. But HLA-27 is sometimes positive in patients with ankylosing spondylitis (males with arthritis of lower spine), juvenile

Fig. 253 Iritis (see Fig. 257).

Fig. 254 Slit-beam view of flare and cells in anterior chamber.

Fig. 255 Keratitic precipitates and posterior synechiae.

rheumatoid arthritis, Reiter’s syndrome (young males with urethritis and conjunctivitis), and inflammatory bowel disease. HLA27 negative causes are toxoplasmosis, sarcoidosis, Lyme disease, influenza, lymphoma, AIDS, herpes simplex and zoster (shingles), and Behc¸et’s disease (ulcers in the mouth and genitals). There are other even rarer etiologies. Therefore, careful clinical judgement is needed in determining the timing and extent of the work-up, taking into consideration cost, severity, chronicity, and associated medical history.

Patients with juvenile rheumatoid arthritis and chronic iritis often develop a band of superficial corneal calcification known as band keratopathy (Fig. 256). It also occurs in sarcoidosis and hypervitaminosis D and may be removed with chelation.

Characteristics to help distinguish iritis from two other important causes of a red eye are given in Fig. 257 on preceding page.

Posterior uveitis (choroiditis)

(Fig. 258)

Posterior uveitis is characterized by white exudates on the retina, sometimes obscured from view by cells extending into the vitreous. It leads to chorioretinal atrophy with pigment mottling (Fig. 259). Often no cause is found, but the following etiologies should be considered.

1Bacterial: syphilis, tuberculosis.

2Viral: herpes simplex, cytomegalovirus in 25% of AIDS patients.

3Fungal: histoplasmosis, candidiasis.

4Parasitic: Toxoplasma, Toxocara.

5Immunosuppression: AIDS predisposes to several of above.

6Autoimmune: Behçet’s disease (mouth and genital ulcers with dermatitis); sympathetic ophthalmia.

Sympathetic ophthalmia refers to a traumatic or surgical injury to the uvea of one eye causing an immune uveitis in the uninvolved eye. A penetrating injury involving

Fig. 256 Band keratopathy.

Fig. 258 Toxoplasma gondii choroiditis often reactivates next to old lesion.

Fig. 259 Old toxoplasmosis scar: sclera visible through atrophic retina and choroid.

Fig. 260 Fish hook in eye.

Fig. 262 Penetrating injury through iris and lens capsule with secondary cataract.

the uvea is referred to as a ruptured globe (Figs 260–262). Handle the eye with minimal probing. Place the patient at rest with bilateral shields that exert no pressure and call the eye surgeon immediately. If the uvea or retina are extruded from the eye and it cannot be repaired, the eye is removed (enucleated). A spherical prosthesis is then placed in the orbit and covered with conjunctiva (Figs 263–265). A removable scleral prosthesis painted to match the other eye is placed on the conjunctiva. Enucleation should be performed within 10 days of the injury to prevent sympathetic ophthalmia. Treatment of choroiditis is directed at the specific cause if one can be found.

Fig. 261 Ruptured globe through sclera and cornea with prolapse of iris and ciliary body.

Fig. 263 Enucleated socket with scleral prosthesis.