electerical injery and other rays to the eyes a.hekmatian md 1387

Electerical Injery and other Rays to the eyes

A.Hekmatian MD1387

a. Very rare cause of cataract, 5% to 20% major electrical injury patients.

b. Most often follows shock to head.

c. Usually more than 1,000-V current.

d. Initial anterior cortical vacuoles, replaced by white opacities.

e. PSCcataract less common.

f. Cataract may present many months after injury.

g. Cataract matures within few years after injury.

Electric shock0

Ultraviolet (UV) rays are part of electro-

magnetic radiation. They are invisible

rays lying beyond the violet end of the

visible spectrum.

Low intensity ofUV rays are also emitted

from fluorescent lamps, TV and

computer monitors.

What are ultraviolet rays?

As different intensity (wavelength) ofUV has different effect on us, they are commonly categorized as UV-A, UV-B and UV-c.

UV-C (wavelengths from 200nm - 290nm) is present above the earth's

atmosphere and also given out from welding arcs. It also arises from sunlight's reflection from snow at high altitude.

UV-B (wavelengths from 290nm - 320nm) and UV-A (wavelengths from 320nm - 390nm) are present in our living environment, from direct sunlight or reflection from snow, water, sands, glass windows, walls etc

Are there different types of UV rays?

I. Clinical features

A. Synonyms.

1. Snowblindness.

2. Welder's arc burn.

3. Keratitis photoelectrica.

4. Ultraviolet (UV) keratopathy)

B. Ocular features.

1. Onset of symptoms usually 8 to 24 hours after exposure and characterized by pain, photophobia, and foreign body sensation.

Ultraviolet Radiation Inju

2. Signs may include eyelid

erythema; tearing,conjunctival

injection, corneal epithelial

irregularities, edema, and

punctate epithelial erosions.

C. Course/prognosis.

1. Signs and symptoms should resolve over 24 to 48 hours.

2. Prognosis for visual recovery is excellent.

3. Chronic UV exposure can lead to pterygia, pingueculae, an cataracts.

D. Complications/sequelae.

1. Any breakdown of corneal epithelium causes eye to be more susceptible to infection, ulceration, and scarring.

2. Also, association exists with conjunctival squamous cell carcinoma.

A. Pathogenesis

1. Clinical findings result from excessive exposure to radiation with wavelength of approximately 290 nm.

2. Exposure to UV radiation results in characteristic changes in cells produced by changes in proteins, including inhibition of mitosis and loss of cellular adhesion.

3. Clinical and pathologic changes evident after 6 to 8 hours of , exposure.

B. Risk factors1. Physical factors.a. Snow can reflect UV light, welder's lamps,

and othersources such as sunlamps, malfunctioning mercury vapor lamps

2. Iatrogenic factors phototherapy for psoriasis or other

medical conditions can cause keratopathy.3. Use of tanning bed without protective

goggles increases risk.C. Epidemiology.1. Fairly common, especially among welders.

A. Slitlamp examination with instillationof fluorescein reveals typical punctate epithelial changes.

B. Palthologic findings.

1. uv waves generally absorbed by conjunctiva and cornea, 'leading to conjunctivitis and keratitis.

C. Differential diagnosis

1. Other causes of punctate staining include dry eye

(keratoconjunctivitis sicca), floppy eyelid syndrome

Diagnosis

A. Oral alnalgesics and pressure patching with antibiotic ointment .Bandage contact lenses also aid with healing

B. Consider treating as corneal abrasion if significant number of punctate epithelial erosiqns present.

C. Preventionl avoidance .

1. Use UV-absorbing glasses or goggles and proper eyewear when welding to prevent this condition,

Management/treatment

D. Monitoring

1. Follow up patients every few days until corneal epithelial defect resolved.

E. Patient education

1. Signs and symptoms generally

resolve in 24 to 48 hours.

2. Remind patient to use UV-protective

eyewear.

I. Clinical featuresA. Clinical description.1. Findings resemble diabetic

retinopathy.B. Signs and symptoms.1. Reduced visual acuity secondary to

macular edema andnon perfusion occurs 6 to 36 months

after treatment.

Radiation Retinopathy

2. Bilateral in one third of.external beam irradiation cases.

3. Early features. a. Microaneurysms.b. Telengiectasia.c. Cotton-wool spots.d. Intraretinal hemorrhages.e. Capillary non perfusion. -f. Retinal edema.g. Hard exudates.

Microaneurysmal changes telangiectasias Edema ; andhemorrhages are temporal to the fovea in OS

4. Late features.a. Vascular sheathing.b. Hard exudates.c. Cystoid macular edema.d. Neovascularization.e. Rubeosis and neovascular

glaucoma.f. Ischemic optic neuropathy.

A. Pathogenesis.

1. On retinal vascular endothelial cellular level,

mitosis arrested and nucleus may degenerate.

2. Initial vascular changes include early swelling

with

degeneration of intima and endothelial cells.

3. Subsequent changes include vascular occlusion

by thrombus formation and fibrosis.

Basics

B. Risk factors

1. Neoplasm involving eye, orbital,

periorbital, nasopharyngeal, face, brain, or

other adjacent tissue, with subsequent

irradiation and inadequate shielding by

technical staff.

a. Fifty percent of patients treated for

nonocular neoplasm.

2. Radiation retinopathy develops

after total doses of 30 to 35 Gy

within 3 to 36 months

(mean time, 18 months).

a. If more than 80 Gy administered,

85% of patients develop radiation

retinopathy within few months.

3. Higher the fraction size, greater the risk of radiation retinopathy.

a. Usual dose for external beam therapy 200 to 300 cGy/day, given over 1- to 2-month period

for total dose of 35 to 72 Gy.

b. Twice as many patients develop radiation retinopathy with 250-cGy fractions than with

200-cGy fractions.

4. Local plaque therapy (brachytherapy)

requires higher doses to produce damage

than external beam therapy(teletherapy).

5. Diabetes mellitus and administration of

chemotherapy, whether concomitant or not,

additive to retinopathic effects of

radiation.

A. Clinical diagnosis.

1. Consider when head or neck radiation given for any reason including metastatic CNS tumors, orbital treatment for thyroid disease, and orbital pseudotumor.

Diagnosis

B. Imaging

1. Fluorescein angiographyshows

capillary nonperfusion.

A.Early phase

(1) Dilated and telangiectatic retinal vessels.

(2) Blocked fluorescence secondary to retinal hemorrhages.

(3) Hypofluorescence secondary

to capillary nonperfusion.

b.laet phase

(1) Leakage from affected retinal vessels

and from neovascularization if present

C. Pathologic findings.

1. Preferential damage to inner retinal

layers resulting in paucity of ganglion

cells.

Photo receptors relatively resistant.

Fluorescein angiogram of the left eyedemonstrates large areas of capillarynonperfusion. The foveal avascular zone isenlarged, and the microaneurysms showleakage.

2. Eosinophilic exudate in outerplexiform layers.

3. Retinal capillary changesincluding fusiform dilations,microaneurysms, and focal

lossof endothelial cells andpericytes.

4. Capillary closure

5. Thickening of retinal bloodvessel walls.6. New blood vessels on surface ofretina or optic disc.7. Intraretinal blood or blood invitreous cavity.8. Peripheral anterior synechiaeand fibrovascular membrane onsurface of iris in eyes withneovascular glaucoma.

D. Differential diagnosis.

1. Diabetic retinopathy.

2. Multiple branch retinal artery

obstruction and embolic disease.

3. Multiple episodes of venous

occlusive disease.

4.Postoperative cystoid macular edema.

5. Sickle cell disease.

6. Peripheral uveitis.

7. Hypertension.

8. Ocular ischemic syndromes.

9. Takayasu disease.

10. Hyperviscosity syndromes and blood dyscrasias.

A. Medical therapy.1. Apply guidelines of Early .Treatment Diabetic

RetinopatpyStudy for macular edema and

neovascularization.

Managementltreatment

2. Macular photocoagulation

effective in decreasing macular

edema; may improve vision.

3. Consider pars plana vitrectomy for nonclearing vitreous hemorrhage.

B. Prevention.

1. Adequate shielding of eye during radiation treatment.

2. If satisfactory shielding not achieved, patient will

receive far larger dose than prescribed by radiation

oncologist .

3. Inadequate shielding considered responsible for cases

of retinopathy after radiation thought of safe dose or in

area thought to pose no threat to ocular tissue .

C. Monitoring.

1. Monitor frequently for

development of retinal

changes.

I. Clinical featuresA. Synonyms.1. Solar retinopathy.2. Eclipse burn.3. Eclipse blindness.4. Eclipse retinopathy.5. Solar retinitis.6. Solar chorioretinal burn.7. Photoretinitis.8. Foveomacular retinitis.

Solar Retinopathy

B. Clinical description.

1. Signs and symptoms.

a. Initial features.

(1) Browache.

(2) Positive central scotoma.

(3) Afterimage.

(4) Chromotopsia.

(5) Metamorphopsia

(6) Decreased visual acuity, usually to 20/200 level.

(7) Small, yellow-grayish

b. Chronic features

(1) Yellow-grayish lesion fades over 2 weeks; replaced by "lamellar hole" or "cyst,“ which produces permanent

red foveal appearance. Red reflex permanent and pathognomonic.

(2) Foveolar depression.

(3) Macular pigmentary disruption can occur with significant solar phototoxicity

b. Chronic features

The OS demonstrates a yellowish lesion at the level of the retinal pigment epitheliumcentered on the fovea.

Yellowish pigment epithelial lesions are seen in the fovea.

Two months later the yellowish lesion has been replaced by a small, focal depression.

Fluorescein angiogram demonstrates a Centra window defect in the macula.

BasicsA. Pathogenesis.

1. Blue light largely responsible for producing photochemical injury by initially damaging apical melanosomes in retinal pigment.

2. Subsequent release of lysosomal

enzymes may occur, with resultant cell damage and degeneration of photoreceptors and RPE.

B. Risk factors.

1. Sun gazing.

a. Illicit drug use.

b. Viewing solar eclipse

c. Occupational (ie, astronomers,

military personnel).

2. Without sun gazing.

a. Increased ocular pigmentation.

b. Increased body temperature,warm

climate, exercise, or infection.

c. Clear ocular media

d. Environmental conditions such

as highly reflective surroundings

and reduced atmospheric ozone.

A. Imaging.

1. Fluorescein angiography.

a. In early stages, leakage of dye occurs through RPE;clinically may appear as yelloWish abnormality seen in fovea·

b. In severe cases, window defect

may be present.

Diagnosis

The right macula reveals an abnormal foveal reflex with a small reddish facet-like eccentric defectwithin the fovea.

Fluorescein angiogram demonstrates a verysubtle window defect centered on the fovea.

B. Pathologic findings.

1. Focal loss of rod and cone nuclei.

2. Disruption of receptor elements in

foveola.

3. In severe cases. RPE

depigmented but intact.

4. Choriocapillaris intact.

C. Differential diagnosis.

1. Early stage-yellow lesion.

a. Central serous chorioretinopathy.

b. Choroidal neovascular membrane.

c. Impending macular hole.

d. Chorioretinal inflammatory disorders.

2. Late stage-red spot.

a. Storage diseases.

b. Macular hemorrhage.

c. Macular hole.

d. Central retinal artery occlusion.

e. Berlin edema.

f. Acute macular neuroretinopathy.

g. Sickle cell retinopathy.

D. Clinical course/prognosis.1. Vision usually returns to 20/40or better within 4 to 6 months.2. Fifty percent of patients regain20/20 visual acuity.3. Permanent foveal or juxtafoveallesion well defined andproduces paracentral scotoma.4. Metamorphopsia may persist.

A. Medical therapy-' -none. B. Prevention.1. Avoid sun gazing andobservation of solar eclipse.

Management/treatment

Operating Microscopelight-induced Retinopathy

Clinical features

1. Signs and symptoms.

a. Initial features.

(1) On first or second postoperative day, patients may report paracentral scotoma and decreased vIsion.

(2) Within 24 to 48 hours

postoperatively, oval or round, yellow-white retinal lesion, 1/2 to 2 DD present.

(3) Lesions located at level of

RPEand outer layers of retina; may be

associated

with overlying serous retinal detachment.

b. Chronic feat

(1) Speckled pattern of pigment clumping

and focal areas of

RPEatrophy develop.

(2) Occasionally chorioretinal folds develop.

C. Fiberoptic light pipe produces

lesion with pigmentary disruption

that is diffuse and lacks well-

defined borders of phototoxic

lesions produced by coaxial

illumination of operating

microscope.

1 month after cataract surgery.ODVisual acuity is 20/50 00. Mottledpigmentation is present inferior to the fovea.Choroidal folds extended horizontallythrough the area of pigmentation. Thesefolds can result from contracture of theretinal pigment epithelium from lightinduceddamage.

OS in the same patient had Cataract surgery performed 10 months previously. Vision IS 20/20. Mottled pigmentation is present inferior and nasal to fovea.

2. Photochemical damage secondary to toxicity

produced by absorption of light and

production of oxygen free radicals that

destroy cell membranes and inactivate

enzymes.

B. Risk factors.

1. Exposure to operating microscope during

ocular surgery and fiberoptic illuminators

used during vitrectomy procedures.

2. Important variables in producing these

macular lesions are intensity of light used

and duration of exposure.

a. Ophthalmoscopically visible

lesions created in pseudophakic rhesus

monkeys in 4 to 7.5 minutes using

highintensity coaxial illumination.

3. Greatest risk of photic injury occurs after

insertion of IOL because media clear and

operating microscope focused on retina.

C. Epidemiology.

1. Operating microscope

maculopathy reported to occur

in 7% of patients undergoing

cataract surgery.

lagnosls

A. Imaging.

1. Fluorescein angiography.

a. Focal area of hyperfluorescence

secondary to leakage seen early

b. Results from disturbance of RPE

tight junctions, producing

breakdown of outer BRB.

Diagnosis

2. With time, window defects become apparent.

3. Occasionally, chorioretinal folds seen angiographically

B. Differential diagnosis.

1. Aphakic/pseudophakic cystoid

macular edema.

2. Choroidal neovascular membrane.

Fluorescein angiogram of the right eyedemonstrates choroidal folds and pigmentarydisturbance.

Pigment epithelial changes are seen at thesite of photic injury.

C. Pathologic findings.

1. Histopathologic findings in

animals exposed to operating

microscope show evidence of

photoreceptor and RPEdamage

greater in macula than

elsewhere.

2. Rods more susceptible than cones.

3. Histologic studies of early

photic lesions show

photoreceptor inner and outer

segment damage, swollen RPE, and disrupted RPEtight

junctions.

A. Medical therapy-none.

B. Prevention-despite following

precautions, retinal injury still

possible.

Managementltreatment

1. Use lowest illumination necessary.

2. Filter light at wavelengths below

450 nm.

3. Reduce length and duration of

patient's exposure to coaxial

illumination by using occluder

when coaxial illumination not essential.