Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma
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Clinical Diagnosis and Management of Ocular Trauma |
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Treatment |
Accidental Hypothermia |
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Treatment of the lid burn: |
It occurs on exposures at high altitudes in snow-storm. |
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• The best emergency measure is to cover the face |
Aviators in open aircraft, in a damaged cockpit or while |
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with sterile dressing or handkerchief. |
bailing out from an aircraft in difficulties can also suffer |
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• In early stage the affected area thoroughly cleansed |
from hypothermia. |
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with saline and surrounding area with soap and |
Clinical lesions: Clinical cases are rare because of |
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water |
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the protection afforded by the richly vascular lids and |
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• All the aseptic measures to be taken while treating |
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the care usually taken of them even in conditions of |
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this patients |
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severe stress and even the temperature of cornea is |
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• Blisters to be fully opened, loose epidermis cut away, |
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3 to 5 degrees less than the other tissues of the body. |
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remnants of signed lashes removed |
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There can be varying degrees of conjunctival |
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• Antibiotic cream applied over the denuded area. |
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hyperemia, corneal erosion or opacity which may |
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Sofratulle dressing applied |
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disappear without any ill effects. Severe bilateral |
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• For full thickness burns of the lids, the only effective |
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ulceration of the cornea leading to permanent opacity |
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treatment is graft |
of the cornea. |
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• Full thickness skin graft should be carried out as |
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an emergency measure. |
Cryosurgery |
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Treatment of the burns of the eye: |
It is used as a therapeutic modality in different cases |
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with varying indications. The effects of the freezing on |
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• Local analgesics avoided owing to their deleritious |
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the various ocular tissues and intraocular fluids depends |
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effect on epithelialization. |
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on the temperature used, the area involved, the length |
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Topical cycloplegics – Atropine eye drops |
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of |
application and the type of cell principally |
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Systemic NSAIDs/Sedatives to achieve comfort |
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concerned. |
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Antibiotics to prevent secondary infection |
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Ocular lubrication for corneal burns |
Clinical lesions: |
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• Glass rod to be passed in the fornices to prevent |
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Conjunctiva: Congestion, edema. |
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the risk of symblepharon or use of symblepharon |
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Muscles and tendons: Edema and hemorrhage |
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ring |
• Sclera: Swelling and separation of scleral fibers seen |
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Conjunctival transposition flap |
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microscopically, no clinically evident change |
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• Corneal leucomatous opacity at later stage can be |
• Ciliary body: Freezing of ciliary body resulting in |
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replaced by corneal graft-PK or LK |
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reduce aqueous humor formation |
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• Amniotic membrane graft or Limbal cell transplant |
• Lens: Freezing of the lens utilised in cryoextraction |
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also has a role to play |
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of the lens |
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• Topical corticosteroids also can be used judiciously |
• Retina and choroid: Adhesive chorioretinal reaction |
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in case to case basis. |
• Vitreous: Vitreous ice balls. |
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HYPOTHERMAL INJURIES |
Ultrasonic Injuries |
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Surgical Hypothermia |
Sound waves (sonic or acoustic energy) which are |
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It occurs in cardiovascular surgery and in neurosurgery |
audible to the human ear produce no recognizable |
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or by immersing the patient in ice packs and cold baths, |
ocular injury. Ultrasonic vibrations above the limits of |
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hearing may produce characteristic biological reactions. |
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supplemented by injection of lytic cock-tail. |
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Besides its diagnostic and therapeutic applications, |
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Clinical lesions: At temperatures far under the |
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ultrasonic energy can produce the following injuries |
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therapeutic range opacities developed in the cornea |
to the eye. |
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and lens associated with widespread cellular and |
CLINICAL LESIONS |
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hemorrhagic changes in the ocular tissues, particularly |
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in the ciliary body and retina. Retinal arteries and veins |
• Eyelids—epilation, ulceration of the skin edema. |
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become indistinct and show a fine stippling of the blood |
• Cornea—slight and transient turbidity and swelling |
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column and the retina becomes pale and optic disc |
in superficial corneal layers, earlier changes are |
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white, however, within two seconds of restoration of |
reversible but the later are irreversible and lead to |
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the circulation the fundus assumes its normal |
necrosis. High intensities of radiation cause necrosis |
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appearance. |
and ulceration of the epithelium, a general |
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Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries) |
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57 |
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thickening of the stroma with the formation of dense |
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Corneal lesions—The commonest lesions are |
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leucomatous opacities. |
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interstitial opacities which can be punctate, striate |
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Lens—Two types of cataract—Cavitation and |
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or diffuse. This type of generalised corneal |
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Thermal. In cavitation cataract a zone of frothy, |
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cloudiness usually clears up in few days. However, |
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spume like turbidity of the deeper layers of the |
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if destructive electrical burn is formed the epithelium |
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cortex around the nucleus. In thermal cataract there |
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may become necrotic and exfoliate and sensation |
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is densely white permanent opacity and it develops |
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may be impaired or lost so that serious ulceration |
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after radiation of high frequency and greater |
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may develop and become recurrent |
and |
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intensity. |
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permanent scar may form. In some cases there can |
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• Vitreous—liquefied irreversibly by a few seconds |
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be purulent infiltration of entire cornea, extensive |
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exposure. |
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necrosis, perforation or phthisis of the globe. |
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Retina and choroid—adhesive chorioretinal |
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adhesion with less damage to the sclera than caused |
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Lesions of the iris and ciliary body—Iris and ciliary |
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by diathermy or by ultrasonic energy of megahertz |
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body show irritative changes in any type of electrical |
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frequencies, retinal edema within 12-24 hours |
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injury. There can be mild and transient iritis, |
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followed by proliferative and pigmentary changes. |
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sometimes widespread synechiae formation with |
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heavy aqueous flare and occasionally hyphema. |
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Electrical Injuries |
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• Lesions of the pupil—Unilateral or bilateral extreme |
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miosis with sluggish or absent reactions, spasm of |
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Electrical injuries are due to passage of an electric |
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accomodation. |
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current through the body and the commonest cause |
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Electric cataract—Lenticular opacities form |
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being direct double contact between two live electric |
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sometime after the accident and is sometimes the |
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conductors or a single contact either direct or by short |
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only finding in cases with electrical injury. Main |
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circuit, between a conductor and the earth so that the |
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changes are localized in the capsule itself and in |
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circuit is completed. The similar effect result on being |
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the immediate cortex underneath the capsule. It |
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stuck by lightning. There is a point of entry and often |
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involves both anterior and posterior surface of lens. |
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of exit of the elctric current causing an electrical burn, |
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There is formation of vacuoles underneath the |
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the passage of current usually produces violent tetanic |
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capsule. The type of opacification varies from slight |
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spasms of the muscles, low voltage currents cause |
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indefinite haze to densely crowded punctate |
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auricular fibrillation and high voltage currents affects |
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opacities. There can be evident polychromatic |
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the central nervous system and lead to loss of |
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lusture seen on the lens. |
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consciousness or death from respiratory failure or |
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• Lesions of the retina and choroid—Retinal edema, |
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cardiac arrest and shock. The high resistance offered |
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papilledema, hemorrhages, traumatic chorioretinitis |
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by the non-nervous tissue accounts for the thermal |
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in the periphery, detachment of the retina, vitreous |
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effects of electric injuries, which may result in immediate |
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opacities. Most dramatic changes are at the posterior |
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coagulation of the proteins of the cells. |
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pole which can be combination of the electric |
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CLINICAL LESIONS |
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current and radiation resulting in macular edema, |
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punctate pigmentary degeneration, cystoid changes. |
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• Lesions of the lids—Typical electrical burn at the |
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Optic nerve—Optic neuritis. |
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point of entry – imprint as a sharply defined necrotic |
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Functional disabilites—Photophobia, blepharo- |
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mark without surrounding hyperemia. Lid burns |
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spasm, transient blindness to permanent bilateral |
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differs from heat burns in that the former are |
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visual loss, concentric contraction of the field, ring |
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painless, dry and aseptic and usually circumscribed, |
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scotoma, absolute central scotoma, disturbance of |
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mainly due to the very high temperatures and short |
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binocular fusion. |
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duration. Electrical gangrene may supervene in the |
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subsequent days or weeks due to circulatory |
LIGHTNING INJURY |
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impairment. |
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Even in fatal cases the body may be unmarked, |
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Lesions of the conjunctiva—There can be |
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substantial damage to the eye in both electrical as |
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In some a deep necrotic burn is formed at the point |
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well as lightning injuries. Minor degree of |
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of entry, |
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conjunctival hyperemia and ciliary injection will |
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In others an arborescent tracery of linear burns |
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invariably occur in each and every case of electrical |
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appears (lightning prints). |
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burn. There can be subconjuctival effusion of blood |
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Mydriasis, partial internal ophthalmoplegia, |
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which is transient and which disappears in few days |
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blindness from optic atrophy, deafness, loss of |
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time. |
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memory, nervous damage. |
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58 |
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Clinical Diagnosis and Management of Ocular Trauma |
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Injury to the retina caused by brilliance of flash |
• Treatment of ocular lesions is on the general |
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plays an inconspicuous part in the total damage, |
principles: Rest, atropine, local heat. |
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retinal damage in the macular area, rupture of the |
Bibliography |
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choroid. |
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1. |
Ophthalmology Clinics of North America by Ferenc Kuhn |
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TREATMENT |
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et al. volume 15, Non mechanical injuries. |
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First and foremost is saving of life. |
2. |
System of ophthalmology by Sir Stewart Duke Elder, Vol. |
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XIV, Injuries, Part 2, Non Mechanical Injuries. |
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• Local burns of the skin of the lids or in the vicinity |
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3. |
Work and the Eye, 2nd edition of Rachel V North, |
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is treated as in case of thermal burns. |
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Woburn MA, Butterworth – Heinemann, 2001;51-74. |
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C H A P T E R
12Radiational Injuries to the Eye
Rupesh V Agrawal (India)
Introduction
Radio and television signals, radar, heat, infrared, ultraviolet, sunlight, starlight, cosmic rays, gamma rays, and X-rays all belong to the electromagnetic spectrum and differ only in their relative energy, frequency, and wavelength. These waves all travel at the speed of light, and unlike sound they can all travel through empty space. The frequencies above visible light have enough energy to penetrate and cause damage to living tissue, damage that can be as minor as a sunburn caused by ultraviolet light or as extreme as the incineration of Hiroshima, Japan, during World War II. Lower frequencies do not penetrate, but can cause eye and skin damage, primarily due to the heat they transmit. The energy of electromagnetic radiation is a direct function of its frequency. The high-energy, high-frequency waves, which can penetrate solids to various depths, cause damage by separating molecules into electrically charged pieces, a process known as ionization. Atomic particles, cosmic rays, gamma rays, X-rays, and some ultraviolet are called ionizing radiation. The pieces they generate are called free radicals. They act like acid, but they last only fractions of a second before they revert to harmless forms. Adjusting the energy of therapeutic radiation can select a depth at which it will do the most damage. Ionizing radiation also does damage to chromosomes by breaking strands of DNA. DNA is so good at repairing itself that both strands of the double helix must be broken to produce genetic damage. Because radiation is energy, it can be measured. There are a number of units used to quantify radiation energy. Some refer to effects on air, others to effects on living tissue. The roentgen, named after Wilhelm Conrad Roentgen, who discovered X-rays in 1895, measures ionizing energy in air. A rad expresses the energy transferred to tissue. The rem measures tissue response. A roentgen generates about a rad of effect and produces about a rem of response. The gray and the sievert are international units equivalent to 100 rads and rems, respectively. A curie, named after French
physicists who experimented with radiation, is a measure of actual radioactivity given off by a radioactive element, not a measure of its effect. The average annual human exposure to natural background radiation is roughly 3 milliSieverts (mSv).
It is reasonable to presume that any amount of ionizing radiation will produce some damage. However, there is radiation everywhere, from the sun (cosmic rays) and from traces of radioactive elements in the air (radon) and the ground (uranium, radium, carbon-14, potassium-40 and many others). Earth’s atmosphere protects us from most of the sun’s radiation. Living at 5,000 feet altitude in Denver, Colorado, doubles exposure to radiation, and flight in a commercial airliner increases it 150-fold by lifting us above 80% of that atmosphere. Because no amount of radiation is perfectly safe and because radiation isever present, arbitrary limits have been established to provide some measure of safety for those exposed to unusual amounts. Less than 1% of them reach the current annual permissible maximum of 50 mSv.
It is therapeutic, accidental, and deliberate radiation that does the obvious damage. There has not been much in the way of deliberate radiation damage since Nagasaki, but accidental radiation exposure happens periodically. Between1945 and 1987, there were 285 nuclear reactor accidents, injuring over 1,550 people and killing 64. The most striking example, and the only one to endanger the public, was the meltdown of the graphite core nuclear reactor at Chernobyl in 1986, which spread a cloud of radioactive particles across the entirecontinent of Europe. Information about radiation effects is still being gathered from that disaster. There have also been a few accidents with medical and industrial radioactivity.
Nevertheless, it is believed that radiation is responsible for less than 1% of all human disease and for about 3% of all cancers. This figure does not include lung cancer from environmental radon, because that information is unknown. The figure could be significant, but it is greatly confounded by the similar effects of tobacco.
60 |
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Clinical Diagnosis and Management of Ocular Trauma |
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Radiation can damage every tissue in the body. |
within three months from vomiting, diarrhea, |
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The particular manifestation will depend upon the |
starvation, and infection. Victims receiving 6-10 Sv all |
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amount of radiation, the time over which it is |
at once usually escape anintestinal death, facing |
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absorbed,and the susceptibility of the tissue. The fastest |
instead bone marrow failure and death within two |
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growing tissues are the most vulnerable, because |
months from loss of blood coagulation factors and the |
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radiation as much as triples its effects during the growth |
protection against infection provided by white blood |
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cells. Between 2-6 Sv gives a fighting chance for survival |
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phase. Bone marrow cells that make blood are the |
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if victims are supported with blood transfusions and |
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fastest growing cells in the body. A fetus in the womb |
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antibiotics. One or two Sv produces a brief, non-lethal |
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is equally sensitive. The germinal cells in the testes and |
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sickness with vomiting, loss of appetite, and generalized |
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ovaries are only slightly less sensitive. Both can be |
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discomfort.It is clearly important to have some idea |
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rendered useless with very small doses of radiation. |
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of the dose received as early as possible, so that |
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More resistant are the lining cells of the body—skin |
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attention can be directed to those victims in the 2- |
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and intestines. Most resistant are the brain cells, because |
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10 Sv range that might survive with treatment. Blood |
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they grow the slowest. |
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transfusions, protection from infection in damaged |
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The relative sensitivity of various tissues gives a good |
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organs, and possibly the use of newer stimulants to |
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idea of the wide range that presents itself. The numbers |
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blood formation can save many victims in this category. |
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represent the minimum damaging doses; a gray and |
Local radiation exposures usually damage the skin and |
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a sievert represent roughly the same amount of |
require careful wound care, removal of dead tissue, |
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radiation: |
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and skin grafting if the area is large. Again infection |
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Fetus |
2 grays (Gy). |
control is imperative. |
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Bone marrow |
2 Gy. |
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Ovary |
2-3 Gy |
Injuries of the Eye due to |
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Testes |
5-15 Gy. |
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Lens of the eye |
5 Gy. |
Ionizing Radiation |
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Child cartilage |
10 Gy. |
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X-rays, beta rays, and other radiation sources in |
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Adult cartilage |
60 Gy. |
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Child bone |
20 Gy. |
adequate doses can cause ocular injury. |
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Adult bone |
60 Gy. |
LIDS |
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Kidney |
23 Gy. |
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Child muscle |
20-30 Gy. |
The eyelid is particularly vulnerable to X-ray damage |
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Adult muscle |
100+ Gy. |
because of the thinness of its skin. Loss of lashes and |
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Intestines |
45-55 Gy. |
scarring can lead to inversion or eversion (entropion |
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Brain |
50 Gy. |
or ectropion) of the lid margins and prevent adequate |
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Notice that the least of these doses is a thousand |
closure. |
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times greater than the background exposure and nearly |
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50 times greater than the maximum permissible annual |
CONJUNCTIVA |
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dosage. The length of exposure makes a big difference |
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Scarring of the conjunctiva can impair the production |
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in what happens. Over time the accumulating damage, |
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of mucus and the function of the lacrymal gland ducts, |
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if not enough to kill cells outright, distorts their growth |
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thereby causing dryness of the eyes. |
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and causes scarring and/or cancers. In addition to |
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leukemias, cancers of the thyroid, brain, bone, breast, |
LENS |
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skin, stomach, and lung all arise after radiation. Damage |
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depends, too, on the ability of the tissue to repair itself. |
X-ray radiation in a dose of 500-800 R. directed toward |
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Some tissues and some types of damage produce |
the lens surface can cause cataract, sometimes with |
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much greater consequences than others. |
a delay of several months to a year before the opacities |
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Immediately after sudden irradiation, the fate of |
appear. |
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the patient depends mostly on the total dose absorbed. |
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This information comes mostly from survivors of the |
Injuries due to Ultraviolet |
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atomic bomb blasts over Japan in 1945. Massive doses |
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incinerate immediately and are not distinguishable |
Radiation |
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from the heat of the source. A sudden whole body |
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dose over 50 Sv produces such profound neurological, |
CORNEA |
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heart,and circulatory damage that patients die within |
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the first two days. Doses in the 10-20 Sv range affect |
Ultraviolet radiation of wave lengths shorter than 300 |
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the intestines, stripping their lining and leading to death |
nm (actinic rays) can damage the corneal epithelium. |
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Radiational Injuries to the Eye |
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This is most commonly the result of exposure to the |
welding arc can also damage the the retinal macula. |
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sun at high altitude and in areas where shorter wave |
There may be permanent decrease in visual acuity. |
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lengths are readily reflected from bright surfaces such |
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The intensity of light, lenght of exposure, and age |
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as snow, water, and sand. |
are all important factors. The older ones are more |
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Exposure to radiation generated by a welding arc |
sensitive, also those who have had cataract surgery |
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can cause welding flash burn, a form of keratitis. |
because filtration of light by the lens is impaired. |
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LENS |
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Injuries due to Infrared Radiation |
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Wavelengths of 300-400 nm. are transmitted through |
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the cornea, and 80% are absorbed by the lens, where |
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Potters may be exposed to this type of radiation. |
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they can cause cataractous changes. |
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Wavelengths greater than 750 nm. in the infrared |
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Epidemiologic studies suggest that exposure to solar |
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spectrum can produce lens changes. |
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radiation in these wavelengths near the equator is |
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La “cataracte des verriers”(glassblower’s cataract) |
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correlated with a higher incidence of cataracts. |
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is an example of a heat injury that damages the anterior |
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They also indicate that workers exposed to bright |
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lens capsule among unprotected artists. Denser |
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sunlight in occupations such as farming, truck driving |
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cataractous changes can occur in unprotected workers |
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and construction work appear to have a higher |
who observe glowing masses of glass or iron for many |
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incidence of cataract than those who work primarily |
hours a day. |
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indoors. |
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Another important factor is the distance between |
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Experimental studies have shown that these wave- |
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the worker and the source of radiation. In the case |
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lengths cause changes in the lens protein, which lead |
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of arc welding, infrared radiation decreases rapidly as |
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to cataract formation in animals. |
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a function of distance, so that farther than 3 feet away |
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from where welding takes place, it does not pose an |
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Injuries due to Visible Radiation |
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ocular hazard anymore but, ultraviolet radiation still |
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does. That is why welders wear tinted glasses and |
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(Light) |
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surrounding workers only have to wear clear ones. |
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When we speak of type of exposure, potters look |
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Visible light has a spectrum of 400-750 nm. If the |
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at their cone packs for very short periods of time in |
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wavelengths of this spectrum penetrate fully to the |
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a repeated way, more often nearing the end of firing; |
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retina, they can cause thermal, mechanical, or photic |
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and also according to the use of other methods for |
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injuries. |
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measuring temperature, like the concomitant use of |
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a thermocouple and a reading device. |
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THERMAL INJURIES |
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So, these “short-term” exposures are spaced by |
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They are produced by light intense enough to increase |
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quite longer “exposure-free” periods and the sum of |
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the former does not correlate with the concept of many |
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the temperature in the retina by 10-20C. |
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hours a day. |
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Lasers used in therapy can cause this type of injury. |
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We have searched the literature pertaining to |
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The light is absorbed by the retinal pigment epithelium, |
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Occupational Health and Safety and have not found |
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where its energy is converted to heat, and the heat |
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a single case of presumed “ceramicist’s or potter’s |
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causes photocoagulation of retinal tissue. |
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cataract”, even if the trade of potter is quite older than |
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MECHANICAL INJURIES |
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the one of glassblower. |
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Therefore, I do not think that any of the above |
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They can be produced by exposure to laser energy |
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types of radiation present a threat to potters. |
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from a Q-switched or mode-locked laser, which |
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It is a good thing, mainly at high temperature, to |
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produces sonic shock waves that disrupt retinal tissue. |
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wear lightly tinted industrial grade safety glasses to |
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PHOTIC INJURIES |
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better visualize cones (ocular ergonomics) and also to |
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reassure those who are more worried. |
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They are caused by prolonged exposure to intense |
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These glasses also offer a better protection than |
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light, which produces varying degrees of cellular |
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typical sun-glasses in case of projection of hot dust |
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damage in the retinal macula without a significant |
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particles from a gas kiln when looking through the |
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increase in the temperature of the tissue. |
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peephole in a soft brick door. |
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Sun gazing is the most common cause of this type |
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By the way with ageing, most if not all of us, will |
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of injury, but prolonged unprotected exposure to a |
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suffer from cataracts of the senile type. |
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62 |
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Clinical Diagnosis and Management of Ocular Trauma |
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The progress or change and the related reduction in |
returning to work in less than two days and 95 percent |
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vision is usually quite slow. |
in less than seven days, some eye injuries are |
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Nuclear sclerosis-an increasing density in the central |
irreversible and permanent visual impairment occurs. |
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mass of protein-causes a myopic change than can be |
This is especially true with infrared and visible spectrum |
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corrected by changing glasses for some years-in many |
(bright light) radiation. Both can penetrate through |
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instances restoring vision to near normal. |
to the retina and—although this is rare—can cause |
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permanent retinal damage, including cataracts, |
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Welding Arc Injuries |
diminished visual acuity, and higher sensitivity to light |
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and glare. |
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And welders are not the only workers at risk. While |
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Eye injuries account for one-quarter of all welding |
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the welding arc is the principal source of UVR, other |
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injuries, making them by far the most common injury |
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workers in the area can sustain eye damage from the |
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for welders, according to research from the Liberty |
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radiation as far as 50 feet away from UVR reflecting |
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Mutual Research Institute for Safety. Those most at |
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off shiny surfaces, concrete, or unpainted metals. To |
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risk for welding-related eye injuries are workers in |
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counteract this reflection, you should install shielding |
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industries that produce industrial and commercial |
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curtains where practical or require that all workers in |
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machinery, computer equipment, and fabricated metal |
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the area wear appropriate eye protection. |
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products. |
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Yet, despite the insidious damage radiation can |
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The best way to control eye injuries is also the most |
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cause, molten and cold metal particles striking the eye |
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simple: proper selection and use of eye protection. |
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are still the most common sources of eye injuries. |
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Helmets alone do not offer enough protection. Welders |
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should wear goggles or safety glasses with sideshields. |
Eye Protection Goes Beyond |
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Goggles provide better protection than safety glasses |
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from impact, dust, and radiation hazards. |
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the Helmet |
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Unfortunately, workers don’t always wear goggles |
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or safety glasses because of low perception of risk, |
Helmets and protective clothing shield welders from |
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poorly maintained lenses, discomfort, having to wear |
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“sunburn” and “welder’s flash,” but with the majority |
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prescription lenses underneath, and vanity. It is |
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of their work performed with the helmet up, welders |
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important to stress to workers that welding-related eye |
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also need to wear goggles or safety glasses with |
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injuries come from a number of sources, including: |
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sideshields. These will protect them from particles sent |
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mechanical damage from being struck by flying |
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flying during pre-job grinding, hammering, and |
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particles and chipped slag; radiation and |
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power chipping that make it past the helmet’s |
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photochemical burns from ultraviolet radiation |
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protective front. |
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(UVR), infrared radiation, and intense blue light; |
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Some guidelines and safety warnings for welding |
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and irritation and chemical burns from fumes |
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suggest workers should not wear contact lenses, even |
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and chemicals. |
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though there does not appear to be any research that |
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To help in reducing eye injuries, you should educate |
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would support such a recommendation. In fact, the |
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workers about all of the dangers they face and should |
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National Safety Council, the American Welding Society, |
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implement an eye protection plan that outlines proper |
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and the FDA all acknowledge that wearing contact |
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welding behavior. |
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lenses while welding is safe and even can provide UV |
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protection. The only caveat is that contact lenses should |
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Cumulative Damage Risks |
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not be used as eye protection in place of safety glasses |
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or goggles. |
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All of the most common types of welding (shielded |
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Once the proper goggles/shields are in hand, you |
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metal-arc or stick welding, gas metal-arc welding, and |
can turn your attention to the type of helmet best suited |
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oxyacetylene welding) produce potentially harmful |
for the job. Published tables are available through the |
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ultraviolet, infrared, and visible spectrum radiation. |
welding helmet vendor or the Internet, which can help |
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Damage from ultraviolet light can occur very quickly. |
you determine the most appropriate lens shade based |
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Normally absorbed in the cornea and lens of the eye, |
on the type of welding and the amperage of the |
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ultraviolet radiation (UVR) often causes arc eye or arc |
welding unit. It is a common misconception that a |
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flash, a very painful but seldom permanent injury that |
darker shade provides more protection against UV. |
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is characterized by eye swelling, tearing, and pain. |
Properly maintained welding helmets, regardless of |
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While most welding-related eye injuries are |
shade, provide 100 percent protection against UV, |
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reversible, with more than half of injured workers |
according to the manufacturers. |
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Radiational Injuries to the Eye |
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63 |
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Arc welding helmets can be fixed shade or variable |
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Now that your workers have the right eye protection |
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shade. Typically, fixed shade helmets are best for daily |
for the job, it is time to implement an ongoing eye |
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jobs that require the same type of welding at the same |
protection plan that ensures they use the equipment |
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current levels, and variable helmets are best for workers |
properly. |
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with variable welding tasks. Helmet shades come in |
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Bibliography |
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a range of darkness levels, rated from 9 to 14 with |
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1. |
Occupational and Environmental Medicine. Joseph |
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14 being darkest, which adjust manually or |
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Ladoue and al, last edition. |
|
||
automatically, depending on the helmet. To determine |
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2. |
Occupational Medicine, Zenz C, 2003. |
|
|||
the best helmet for the job, select a lens shade that |
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3. |
Oshline and Nioshtic database, 2004. |
|
|||
provides comfortable and accurate viewing of the |
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||||
4. |
Precis de Medecine du Travail, Desoille H, Scherrer J, |
|
|||
“puddle” to ensure a quality weld. |
|
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Truhaut R, last edition. |
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C H A P T E R
13Traumatic Angle Recession
Glaucoma: An Overview
Cyres K Mehta, Keiki Mehta (India)
This chapter deals with blunt trauma to the eyeball leading to angle recession glaucoma.
Synonyms: Angle-recession glaucoma, posttraumatic angle recession glaucoma, contusion angle recession glaucoma, contusion angle deformity.
History
Treacher Collins described the micropathology of angle recession glaucoma as a “split into the ciliary muscles in its entire circumference so that angle of the chamber was prolonged out”. In 1945 D’Ombrain postulated that angle recession led to increased intraocular tension.
Angle recession may be associated with many other conditions associated with the ocular trauma sustained such as, such as dislocation or subluxation of the lens, traumatic cataract, iridodialysis, cyclodialysis, hyphema and retinal detachment, extraocular muscle avulsion,orbital trauma and globe rupture in extreme cases.
When Blunt (non-penetrating) injury is sustained by the eye by an object moving parallel to the visual axis,the cornea and anterior sclera is displaced backwards. This leads to a compensatory equatorial expansion. Aqueous and vitreous are relatively incompressible and transmit the force so that the ocular tissues undergo sudden expansion and possibly tearing.
The General features of non-penetrating trauma are (Campbells classification of the 7 tissue rings).
1.Pupillary sphincter tears.
2.Iridodialysis.
3.Anterior ciliary body tear—We can have a angle recession or a tear in the face of the ciliary body. The rupture of the ciliary body between its longitudinal and circular fibers shows that this is the weakest portion of the ciliary body.This leads to deepening of the Anterior chamber also known as angle recession.
4.Cyclodialysis, or a separation of the ciliary body from the sclera.
5.Trabecular dialysis or a tear through the trabecular meshwork.
6.Tearing of the lens zonules leading to phacodonesis, iridodonesis, subluxation or total dislocation of the lens backwards.
7.Retinal dialysis at the ora or a giant retinal tear. After blunt trauma to the globe we can divide
pressure fluctuation into EARLY (few days to few weeks) and LATE (few weeks and later). Intraocular pressure (IOP) may be reduced because of 2 reasons.
Firstly due to to trauma to the ciliary body the amount of aqueous secretion is reduced and secondly due to a total tear of the trabecular meshwork into Schlemms canal the aqueous outflow is greatly exaggerated, or, due to a cylodialysis developing the aqueous is been drained out via uveoscleral ouflow.
Alternatively in the short-term the pressure can rise up for several weeks.This is due to increased resistance to the outflow of aqueous due to trabeculitis (swelling of the meshwork) due to circulating cytokines and prostaglandins.Treatment with corticosteroid is advocated here.
Late Post-traumatic Glaucoma:
Angle Recession Glaucoma
INTERNATIONAL INCIDENCE
In 60-94% of cases of patients with blunt ocular injury in Africa angle recession was noted.
In Africa angle recession glaucoma was frequently bilateral.
The presence of angle recession does not necessarily mean the onset of raised IOP and nerve head pathology.
Other studies have indicated that 6-20% of all individuals with angle recession went on to develop late onset glaucoma.
Again another study showed a 5-8% conversion to glaucoma after angle recession.
A 3:1 to 4:1 male preponderance was noted by some studies.
|
Traumatic Angle Recession Glaucoma: An Overview |
|
65 |
|
INDIAN INCIDENCE (ACCORDING TO |
Also a descemets like membrane is seen growing from |
|
||
SIHOTAAND SOOD) |
the cornea over the angle similar to the membrane |
|
||
Of all traumatic glaucoma patients, 71% were below |
seen in iridocorneal endothelial syndrome. |
|
||
30 years of age. There was a 90% male preponderance |
Chandler claimed that glaucoma is due to |
|
||
Blunt trauma was the mode of injury in 85% of cases. |
impairment of the action of ciliary muscles,due to the |
|
||
|
The cricket ball, tennis ball, gilli-danda (a small flying |
tear in its body, which open the pore of the trabecular |
|
|
stick), hockey stick, bamboo stick and stone were |
meshwork |
|
||
responsible for 30% cases; fire cracker injury in 20% |
Cases with involvement of lesser area of angle |
|
||
cases and 50% were work-related, assaults or accidental |
showed no rise of intraocular pressure during the follow |
|
||
injury. In eyes having angle recession, two or more |
|
|||
up period. This agrees with the findings of Alter who |
|
|||
quadrants were involved in 87% cases. Other features |
|
|||
observed glaucoma to be associated more commonly |
|
|||
of trauma like sphincter tear, hyphema, iridodialysis, |
|
|||
in cases having 240 degrees or more of angle |
|
|||
subluxation, dislocation, vitreous hemorrhage, retinal |
|
|||
involvement. |
|
|||
detachment, and cataract could be seen in various |
|
|||
It is usually agreed that more than 180 degrees |
|
|||
combinations in about 95% cases. Fifty percent of |
|
|||
of angle involvement are required for pressure |
|
|||
traumatic glaucomas had an IOP of =30 mm Hg and |
|
|||
elevation in most cases. |
|
|||
56% had a vision =20/200. |
|
|||
|
|
Its interesting to note that that the other eye in |
|
|
SLITLAMP FINDINGS |
unilateral angle recession glaucoma are more likely to |
|
||
The chamber appears deeper than the other eye.Other |
have elevated IOP as well as be steroid responders. |
|
||
features of blunt trauma such as phacodonesis, |
Its safe to conclude that eyes with a tendency to |
|
||
iridodialysis and hyphema might be seen. |
develop higher IOP have a greater tendency to develop |
|
||
GONIOSCOPIC FINDINGS |
glaucoma after blunt trauma. |
|
||
|
|
|
||
Gonioscopically angle recession is characterized by |
|
|
|
|
widening of the ciliary body and prominence of the |
|
|
|
|
cilary spur. Sometimes trabecular meshwork tears are |
|
|
|
|
seen along with iridodialysis and cyclodialysis. |
|
|
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|
|
After the injury scar tissue may fill the angle |
|
|
|
recession cleft confounding the diagnosis at later follow |
|
|
|
|
ups, so, as soon as blunt trauma is noted and the cornea |
|
|
|
|
is clear enough and the patient cooperative enough |
|
|
|
|
a gonioscopy should be carried out. |
|
|
|
|
FURTHER INVESTIGATIONS |
|
|
|
|
Ultrasound Biomicroscopic Study and or |
|
|
|
|
Anterior Segment OCT |
|
|
|
|
• Ultrasound biomicroscopy produces high-resolution |
|
|
|
|
|
images of the anterior segment, providing cross- |
|
|
|
|
sectional views of the angle in vivo similar to those |
|
|
|
|
of a histologic section. |
|
|
|
• |
This noninvasive procedure is readily performed |
|
|
|
|
in a clinical setting in an intact globe. |
|
|
|
• |
High-resolution images of angle recession, irido- |
|
|
|
|
dialysis, and cyclodialysis have been described. |
|
|
|
• Anterior segment OCT is another modern diagnostic |
|
|
|
|
|
tool which can study the angle (Ziess Visante and |
|
|
|
|
others). |
|
|
|
Pathology
After the initial injury to the ciliary body and or trabe- |
|
cular meshwork, scarring occurs, causing obstruction. |
Figs 13.1A and B: Traumatic glaucoma |
