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Electerical Injery and other Rays to the eyes

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Presentation on theme: "Electerical Injery and other Rays to the eyes"— Presentation transcript:


2 Electerical Injery and other Rays to the eyes
A.Hekmatian MD 1387


4 Electric shock0 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.

5 What are ultraviolet rays?
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.

6 Are there different types of UV 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

7 Ultraviolet Radiation Inju
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.

8 2. Signs may include eyelid
erythema; tearing,conjunctival injection, corneal epithelial irregularities, edema, and punctate epithelial erosions.

9 C. Course/prognosis. 1. Signs and symptoms should resolve over to 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.

10 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.

11 B. Risk factors 1. 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.


13 Diagnosis 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

14 Management/treatment
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,

15 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.

16 Radiation Retinopathy
I. Clinical features A. Clinical description. 1. Findings resemble diabetic retinopathy. B. Signs and symptoms. 1. Reduced visual acuity secondary to macular edema and non perfusion occurs 6 to 36 months after treatment.

17 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.

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

19 4. Late features. a. Vascular sheathing. b. Hard exudates. c. Cystoid macular edema. d. Neovascularization. e. Rubeosis and neovascular glaucoma. f. Ischemic optic neuropathy.


21 Basics 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.

22 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.

23 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.

24 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.

25 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.

26 Diagnosis 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.

27 B. Imaging 1. Fluorescein angiographyshows capillary nonperfusion. A.Early phase (1) Dilated and telangiectatic retinal vessels. (2) Blocked fluorescence secondary to retinal hemorrhages.

28 (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.

29 Fluorescein angiogram of the left eye
demonstrates large areas of capillary nonperfusion. The foveal avascular zone is enlarged, and the microaneurysms show leakage.

30 2. Eosinophilic exudate in outer
plexiform layers. 3. Retinal capillary changes including fusiform dilations, microaneurysms, and focal loss of endothelial cells and pericytes. 4. Capillary closure

31 5. Thickening of retinal blood
vessel walls. 6. New blood vessels on surface of retina or optic disc. 7. Intraretinal blood or blood in vitreous cavity. 8. Peripheral anterior synechiae and fibrovascular membrane on surface of iris in eyes with neovascular glaucoma.

32 D. Differential diagnosis.
1. Diabetic retinopathy. 2. Multiple branch retinal artery obstruction and embolic disease. 3. Multiple episodes of venous occlusive disease.

33 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.


35 Managementltreatment
A. Medical therapy. 1. Apply guidelines of Early . Treatment Diabetic Retinopatpy Study for macular edema and neovascularization.

36 2. Macular photocoagulation
effective in decreasing macular edema; may improve vision. 3. Consider pars plana vitrectomy for nonclearing vitreous hemorrhage.

37 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 .

38 C. Monitoring. 1. Monitor frequently for development of retinal changes.


40 Solar Retinopathy I. Clinical features A. Synonyms.
2. Eclipse burn. 3. Eclipse blindness. 4. Eclipse retinopathy. 5. Solar retinitis. 6. Solar chorioretinal burn. 7. Photoretinitis. 8. Foveomacular retinitis.

41 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

42 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

43 b. Chronic features Yellowish pigment epithelial lesions
are seen in the fovea. The OS demonstrates a yellowish lesion at the level of the retinal pigment epithelium centered on the fovea.

44 Two months later the yellowish lesion
has been replaced by a small, focal depression. Fluorescein angiogram demonstrates a Centra window defect in the macula.

45 Basics A. 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.

46 B. Risk factors. 1. Sun gazing. a. Illicit drug use. b. Viewing solar eclipse c. Occupational (ie, astronomers, military personnel).

47 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.

48 Diagnosis 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.

49 The right macula reveals an
abnormal foveal reflex with a small reddish facet-like eccentric defect within the fovea. Fluorescein angiogram demonstrates a verysubtle window defect centered on the fovea.

50 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.

51 C. Differential diagnosis.
1. Early stage-yellow lesion. a. Central serous chorioretinopathy. b. Choroidal neovascular membrane. c. Impending macular hole. d. Chorioretinal inflammatory disorders.

52 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.

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


55 Management/treatment
A. Medical therapy-' -none. B. Prevention. 1. Avoid sun gazing and observation of solar eclipse.

56 Operating Microscope light-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.

57 (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.

58 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.

59 1 month after cataract surgery.OD
Visual acuity is 20/ Mottled pigmentation is present inferior to the fovea. Choroidal folds extended horizontally through the area of pigmentation. These folds can result from contracture of the retinal pigment epithelium from lightinduced damage. 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.

60 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.

61 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.

62 C. Epidemiology. 1. Operating microscope maculopathy reported to occur in 7% of patients undergoing cataract surgery.


64 Diagnosis 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.

65 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.

66 Fluorescein angiogram of the right eye
demonstrates choroidal folds and pigmentary disturbance.

67 Pigment epithelial changes are seen at the
site of photic injury.

68 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.

69 3. Histologic studies of early
photic lesions show photoreceptor inner and outer segment damage, swollen RPE, and disrupted RPEtight junctions.

70 Managementltreatment
A. Medical therapy-none. B. Prevention-despite following precautions, retinal injury still possible.

71 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.


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