Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma
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to the secondary glaucoma. Latent and rare |
and these features are its virtue from the military point |
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complication of mustard gas action may be irreversible |
of view. Usually impurities give it brown coloring and |
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superficial corneal opacification, requiring keratoplasty, |
odor similar to that of geraniums. Which can be |
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and/or recurrent conjunctivitis, keratitis, and blepharitis |
undetectable in the battlefield. Lewisite, similarly to |
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(AmedP-6). An effect on the cornea is tetraphasic: |
mustard gas, penetrates clothes, mucous membranes, |
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loosening of the epithelial intercellular junctions, |
and skin. As it contains arsenic atom, lewisite disturbs |
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damage of stromal collagen, stimulation of the stromal |
cellular energetic processes, blocking –SH groups in |
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neovascularizing factor, and apoptosis of endothelial |
pyruvate dehydrogenase and inhibiting acetylco- |
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cells. |
enzyme A synthesis. |
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Ocular symptoms herald other consequences of |
Lewisite produces severe ocular injuries. The first |
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the contamination. They include: chemical skin burns |
sign of ocular injury is painful blepharospasm, followed |
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with blisters, rhinorrhea, vocal cords injury with |
by: chemosis and blepharoedema, keratitis and iritis |
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hoarseness or aphonia, increased mucus secretion in |
with hypopyon within 1 hour after the contact. |
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the airways, bronchospasm, persisting cough, nausea |
Inflammation usually resolves but the necrosis of |
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and vomiting, diarrhea. Other squeals include: skin |
conjunctiva, corneal opacification, corneal pannus, |
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hyperpigmentation or discoloration, painful ulcerations |
secondary glaucoma, and cataract may persist after |
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of the skin, aphonia or chronic hoarseness, chronic |
severe injury. |
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obturative pulmonary disease (COPD), intestinal |
Intensive pain of eyeballs, skin and blisters filled |
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hemorrhage and perforation, aplastic anemia, |
with liquid toxic for not only surrounding tissue but |
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leucopenia, depression, loss of libido, anxiety. It was |
also for medical staff is characteristic for lewisite |
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also found that mustard gas increases the risk of |
contamination. It exerts a severe irritating effect on |
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pulmonary carcinoma in chemical causalities and |
the airways, forcing the immediate use of anti-gas |
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manufacturers (Norman 1975, Woda et al 1968). It |
facemask. Lewisite absorbed to the circulating blood, |
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should be born in mind that general symptoms, such |
mainly through the respiratory tract, causes hemolytic |
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as headache and abdominal pain, nausea and |
anemia, increased capillary permeability, pulmonary |
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vomiting, anemia, and leucopenia may be identical |
edema, damage of both liver and kidneys, and |
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with those in radiation sickness. |
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hypovolemic shock. |
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Basic medical management of chemical causalities |
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The treatment includes copious eye irrigation with |
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is careful washing of skin and irrigation of eyes as well |
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water and normal saline. Topical antibiotic ointments, |
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as removal of the contaminated clothes. Eyes and |
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strong mydriatics (atropine solutions) are used. An |
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mucous membranes are washed with water or normal |
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important element of the treatment is BAL – British |
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saline and sodium bicarbonate for at least 2 minutes, |
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Anti Lewisite (dimercaptol) – chelating arsenic and |
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immediately after contamination with mustard gas |
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liberating –SH groups of pyruvate dehydrogenase. It |
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(Wilems 1989). Delayed eye irrigation is useless as |
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is used topically in the form of ophthalmic ointment, |
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mustard gas is already absorbed. Mustard gas is |
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skin ointment, and systematically in intramuscular |
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removed from the skin wooden spatula, when |
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injections. |
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contaminated clothing was removed, and powdered |
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iii.Phosgene oxime: Phosgene oxime, being |
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with anti-gas powder (calcium chloride or magnesium |
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oxide). Activated carbon and synthetic resins may also |
classified as blister agent (vesicant), has an irritating |
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be used for this purpose(Smith et al 1991). Then, |
action without producing the blisters. It is solid |
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exposed skin is washed with water and soap and |
compound dispersed in the form of aerosol for military |
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normal saline. Treatment of ocular injuries include |
purposes. Mechanism of its action is not clearly |
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application of topical antibiotic ointments, |
explained, but most probably it damage protein and |
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corticosteroids, and mydriatics for dozens weeks to |
enzyme structures. Contact with the eyes causes edema |
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several months (Safarinejad et al 2001). Then, the |
of the conjunctiva and keratitis, leading to its |
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patients are followed-up for months to detect possible |
opacification and marked decrease in visual acuity. |
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corneal and anterior chamber symptoms. Wartime |
Typical for phosgene oxime action are skin lesions in |
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practice indicates, however, that for the treatment |
the form of reddening and urticaria progressing to the |
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severity of injuries, depending on the dose and rapid |
skin necrosis with suprainfections. Medical management |
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decontamination is more important than medical |
includes decontamination with water and sodium |
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procedures. |
bicarbonate. Then, topical antibiotics and preparations |
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ii. Lewisite: Lewisite was synthesized in by WL Lewis |
accelerating the healing of cornea and skin are applied. |
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3. Remaining military toxic agents: One should |
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in USA in 1918 (it was named after him). Most |
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probably it was not used as chemical warfare agent |
remember that each case of the conjunctival irritation |
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up-to-now. Pure lewisite is colorless and odorless liquid |
manifested by reddening, burn sensation or lacrimation |
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308 |
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Clinical Diagnosis and Management of Ocular Trauma |
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requires facial mask wearing and detecting procedures. |
These plants may serve as food or shelter in the natural |
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Such symptoms may be the first sign of battlefield |
terrain configuration. The most toxic proved purple |
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contamination with deadly substances. These |
agent and orange agent, containing high levels of |
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substances include: lung damage agents (phosgene, |
dioxins. |
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diphosgene, chlorine, chlorpicrin), cyanide compounds |
3. Incendiary agents: They serve to eliminate |
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(hydrogen cyanide, cyanogen halides, cyanogens |
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mankind and damaging the equipment and objects |
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chloride, cyanogens bromide). Every case of paralyzing |
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(flammable aluminum and phosphorous compounds, |
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agents use – both depressants, tranquillizers and |
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hydrocarbon fuels: gasoline, refuel, fuel oil, kerosene). |
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stimulants, hallucinogens (LSD, amphetamines) – |
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These agents cause ocular, skin and mucous mem- |
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papillary dilatation is |
seen together with typical |
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branes burns, and combustion gases are additionally |
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neurological symptoms. |
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toxic for respiratory tract and central nervous system. |
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Military auxiliary agents |
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i. Thermal ocular burns: In wartime, thermal |
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To this group of agents belong: lacrimators, defoliants, |
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ocular burns result from the use of incendiary agents, |
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incendiary agents, and smoke screen. In general, these |
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incendiary bombs, flames of exploding shells and fire. |
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agents do not cause direct irreversible immobilization |
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Military thermal burns do not differ from the typical |
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of the enemy and according to the international law |
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eye burns, described elsewhere, except the presence |
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are approved for use, except defoliants, dioxan, and |
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of gunpowder remnants or foreign bodies connected |
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incendiary bombs. |
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with the explosion. However, ocular burns with |
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1. Lacrimators and smoke screens: Lacrimators |
phosphorus need separate discussion. |
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(tear gas, pepper gas) are military gases irritating the |
ii. Burns caused by phosphorus: White phos- |
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eye and upper respiratory tract. They rapidly and |
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phorus is used in the phosphorus incendiary bombs. |
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transiently cause stinging sensation and, tearing (for |
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It is self-ignition agent, which produces white fumes |
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about 15 minutes), and reddening (for about 30 |
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in the air. White phosphorus is a cause of numerous |
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minutes) of the eyes, reddening of the eyelids (for about |
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and deep burns of the skin and eyes. Therefore, |
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1 hour) without toxic consequences. Rarely, the |
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immediate decontamination is of utmost importance. |
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corneal epithelium is damaged. Ocular symptoms are |
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The particles of white phosphorus are mechanically |
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accompanied by the cough and rhinorrhea. Similar |
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removed from the eyelids, conjunctiva and cornea. |
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but weaker effects are produced by the smoke screens, |
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The eye and exposed skin are abundantly washed with |
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used to mask location of the military troops or in shock |
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1% copper sulfate solution or 5% sodium bicarbonate, |
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tactics. These agents serve not only as warfare agents |
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which neutralize phosphorus. Then, abundant irrigation |
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but also as riot control agents used by police forces. |
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with water or normal saline is necessary. It not only |
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Medical management includes: eye irrigation with water |
cleans and cools the tissue but also removes copper |
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and possible use of topical antibiotics. Chlorine |
compounds, preventing general intoxication. Medical |
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derivatives (calcium hypochlorite) are banned as their |
treatment involves topical antibiotic use, epidermization |
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chemical reactions with lacrimators may produce toxic |
preparations, mydriatics, and corticosteroids later. |
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effects. |
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2. Dioxins and defoliants: Dioxins chemically damage the skin, mainly on the face and hands, manifested as chloracne, leaving deep, sometimes disfigurating scars. As far as the eyes are concerned, dioxins may produce deformity of the eyelids, leading to the recurrent conjunctivitis and marginal blepharitis. Skin lesions persist for years and may be accompanied by the lesions to pancreas, liver, and immunological system, anemia, and neurological diseases. The bestknown dioxin is TCDD. Its mechanism of action and treatment of poisoning are unknown. Actually, cases of Dixon poisoning are rare and are related only to terrorist attacks or intelligence actions. During the wars in Korea and Vietnam, several cases of poisoning with dioxins being added to defoliants were noted in both participants of the conflict. Defoliants are phytotoxic chemicals used to remove plants in the battlefields.
Biological Warfare
Biological warfare agents consist of microorganisms and their toxins. These agents serve for permanent elimination of the enemy, quite often with mortal effect. International agreements concerning the ban of biological weapons are similar to that concerning chemical weapons and were agreed upon in 1925 and 1972. Despite of biological weapons ban, several countries still experiment with biological weapon, which is also within the interest of terrorist organizations (socalled bioterrorism).
The following warfare agents are considered mortal: botulin toxin (BTX), SEB toxin (staphylococcal enterotoxin type B – cadaveric poison), antrax, tularemia. Brucellosis, Q fever, VEE fever incapacite the enemy. Out of all types of the biological warfare agents, characteristic ocular signs are produced by the botulin
Ocular War Injuries |
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309 |
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toxin, produced by Clostridium botulinum. It inhibits |
absorbed energy. Penetrating radiation is produced |
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acetylcholine release in the myoneural endings and |
during nuclear explosion, lasts for dozen seconds, and |
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parasympathetic nerves. Ocular symptoms include: |
is composed of electromagnetic gamma rays and |
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papillary dilatation, accommodation disorders and |
neutron radiation. Radioactive pollution is related to |
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double vision. The general symptoms include: mouth |
the radioactive dust fallout after explosion and |
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dryness, peristalsis impairment, speech and swallowing |
radioactive substances formation by the neutron |
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disorders, breathing muscles paralysis. Antitoxin is used |
radiation. It results in X, gamma, alpha, beta, and |
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in the treatment. Mortality rate in untreated subjects |
proton rays emission, the most intense during a few |
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is about 65% in about 18 to 36 hours. |
days but persisting for years. |
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Radiation sickness may develop within hours after |
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Nuclear Warfare |
nuclear explosion. However, it should be born in mind |
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Nuclear weapon is characterized by the most |
that now, when the nuclear weapons are banned, |
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symptoms of radiation sickness may result from |
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destructive action, out of all types of weapons. Its effect |
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inappropriate storage of the radioactive substances, |
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on the vision is connected with five elements of |
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leak of nuclear reactors cooling water, overheating or |
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explosion: blast, thermal radiation, shock wave, |
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explosion in the nuclear power plants. General |
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penetrating radiation, and radioactive pollution. Data |
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symptoms of the radiation sickness include: headache, |
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on the nuclear warfare effects on the human body |
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abdominal pain, nausea, vomiting, gastrointestinal |
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come from the end of the II World War, when USA |
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hemorrhage, skin burns. Later, anemia and leucopenia |
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dropped the atomic bombs on the Japanese cities |
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develop. Ocular effects of the radiation sickness include |
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Hiroshima and Nagasaki (on the 6th and 9th August |
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edema and reddening of eyelids with madarosis. |
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1945). Other nuclear explosions were related to the |
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Blisters on the eye lids skin, necrotic conjunctival |
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nuclear weapons testing carried out by several countries |
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ulceration, corneal erosion, and corneal stroma |
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during so-called Cold War. It should be assumed that |
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infiltrations follow. Ultimately, eye lids scar deformities, |
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such tests did not involve experiments on human |
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conjunctival adhesions, corneal defects with perforation |
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beings. The Cold War arming was followed by the |
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are observed. Typical sequel is postradiation cataract |
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period of nuclear disarmament. In 1963, United States, |
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that may develop from 3 months, already (Sinskey |
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Soviet Union, and Great Britain Kingdom signed an |
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1955). It begins with punctate dot opacification in the |
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agreement which banned testing in the atmosphere, |
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front of the posterior lens capsule, progressing to the |
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outer space, and underwater. However, tests |
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subcapsular discoid changes, and finally involves the |
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underground tests were permissible. In 1968, an |
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whole lens (Ham et al 1953). Patients with general |
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agreement on nuclear weapons non-proliferation, |
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symptoms of the radiation sickness manifested by |
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signed by 178 countries, and prolonged open-ended |
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hematopoietic disorders but without visible ocular |
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in 1995. A comprehensive test ban was approved by |
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problems require periodical eye fundus examination |
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UN General Assembly in 1996; 170 nations have now |
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signed. Actually, China, France, Russia, United States, |
to detect possible intraretinal and preretinal |
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Great Britain, India, and Pakistan have nuclear |
hemorrhages, hemorrhages into vitreous. |
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weapons. Moreover, it is stored in post-Soviet regions: |
OCULAR WAR INJURIES RELATED TO THE |
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Bielarus, Kazkhstan, and Ukraine. It is probable that |
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also Israel and Iran have nuclear weapons. |
LASER LIGHTAND EXPLOSION BLASTS |
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There are several typical ocular injuries in nuclear |
Accidental laser use and explosion blasts produce |
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explosion survivors. Intensive light during nuclear |
electromagnetic wave of the visible light, similar to |
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explosion causes transient central vision disturbances. |
infrared light harmful for the macula. It results in the |
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Thermal radiation, related to the blast, produces eye |
central vision disturbances, manifested by the visual |
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burns and lens opacification. This problem is discussed |
acuity decrease, central scotoma and color sensitivity |
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in detail within the effects of explosion blast and laser |
disorders. Mechanism of these pathologies involves |
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light. Shock wave means translocation of air with |
photochemical macular metabolism disorders with |
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supersonic speed and it is not produced in case of |
accompanying small foci of the internal structures |
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neutron bomb explosion. Shock wave may cause |
edema and intraretinal blood extravasation. Listed |
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mechanical injuries related to the foreign bodies in the |
disorders may persist for about 1 to 3 months. Lesions |
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eye and circulatory disorders due to the sudden change |
to the macular pigmentary epithelium and its outer |
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of the air pressure (Flick 1948). |
structures are also possible (Harris et al 2003). The |
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Nuclear explosion produces penetrating radiation |
later occur, if the electromagnetic wave mainly consist |
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and radioactive pollution. Both may produce similar |
infrared light, being a component of laser light, falling |
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disorders known as radiation sickness. Ocular and |
vertically on the eye. Laser light falling on the eye under |
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systemic clinical effect will depend on the dose and |
certain angle causes local skin, conjunctival and corneal |
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310 |
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Clinical Diagnosis and Management of Ocular Trauma |
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lesions. Explosion blast is accompanied by thermal |
14. |
Heier JS, Enzenauer RW, Wintermeyer SF, et al. Ocular |
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radiation which causes eyelids skin, conjunctival and |
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injuries and diseases at combat hospital in support of |
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corneal burns as well as lens opacification (Harris |
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Operations Desert Shields and Desert Storm, Arch |
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et al 2003, Pariselle et al 1988). Prophylactic measures |
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Ophthalmol. 1993; 111(6): 795-8. |
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15. |
Homblass A. Eye injuries in the military. Int Ophthalmol |
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include wearing of goggles, first of all. In the treatment |
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Clin 1981; 21: 121-38. |
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topical anti-inflammatory agents are applied. One |
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16. |
Ko¿uchowska I. Injuries of globe and adnexa. In: Witold |
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should also consider the administration of anti- |
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Or³owski (Ed): Modern Ophthalmology vol. II, PZWL, |
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edematous drugs, such as carbonic anhydrase |
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Warsaw, 1986. |
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inhibitors. In more severe cases corticosteroids are |
17. |
Kuhn F, Morris R, Witherspoon D, Heimann K, Jeffers |
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injected periorbitally. Periodical ophthalmologic follow- |
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J, Treister G. A standardized classification of ocular |
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up central vision examinations are also necessary, |
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trauma. Ophthalmology. 1996; 103:240–243. |
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18. |
Mader TH, Aragones JV, Chandler AC, et al. Ocular and |
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including visual acuity, color and contrast sensitivity, |
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ocular adnexal injuries treated by United States military |
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Amsler test, computer-assisted perimetry. Additional |
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ophthalmologists during Operations Desert Shield and |
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tests and examinations should also be considered: |
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Desert Storm, Ophthalmology. 1993; 100 (10): 1462-7. |
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fluorescein angiography, optical coherence |
19. |
Mariak Z, Mariak Z, Stankiewicz A, ¯ywalewski J. The |
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tomography, electrophysiological tests. |
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occurence of posttraumatic lesions of cranial nerves. |
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Okulistyka, 2002, 2:143–47. |
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20. |
Muzaffar W, Khan MD, Akbar MK, et al. Mine biust |
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4-9, 96. |
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28. |
Solberg Y, Alcalay M, Belkin M. Ocular injury by mustard |
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8. |
Dabrowska Ml. Sulfur mustard induces apoptosis and |
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gas, Surv Ophthalmol. 1997; 41(6): 461-6. |
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necrosis in endothelial cells, Toxicol Appl Pharmacol. |
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29. |
Szaflik J, Langwiñska-Woœko E, Kiciak Z. Blunt okular |
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1994; 141; 568-83. |
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trauma. Okulistyka, 1998, 4:11-15. |
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9. |
Flick J.J. Ocular lesion following the atomic bombing of |
30. |
Willems JL. Clinical management of mustard gas |
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Hiroshima and Nagasaki, Am J Ophthalmol. 1948; 31; |
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casualties, Ann Med Milit Belg, 1989; 3(suppl): 1-61. |
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137-54. |
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31. |
Thach AB, Johnson AJ, Carroll RB. Severe eye injuries |
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10. |
Fryczkowski P, Kmera-Muszyñska M, Kamiñska A. |
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in the war in Iraq, 2003-2005, Ophthalmology. 2008; |
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Classification of mechanical ocular trauma. Birmingham |
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115(2): 377-82. |
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Eye Trauma Terminology (BETT), Okulistyka 2003, 4: |
32. |
Wac³awiak-D¹browska M, Prost M, Kuliñski J. |
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9-15. |
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Posttraumatic choroidal ruptures and retinal dialysis in |
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11. |
Goœ R, Goœ A. Ocular war injuries. Lekarz Wojskowy, |
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technician during service in Iraq – case report. Polski |
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2001, 77 (2): 115-17. |
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Przegl¹d Medycyny Lotniczej, 2007, 13: 445-454. |
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12. |
Ham WT, Richmont VA. Radiation cataract, Arch |
33. |
Ward DL, Gorie C. Occupational eye injuries in soldiers, |
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Ophthalmol. 1953; 50; 618-43. |
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J Occup Med 1991; 33(5): 646-50. |
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13. |
Harris MD, Lincoln AE, Amoroso PJ, At al. Laser eye |
34. |
Woda S, Nishimoto Y, Miyanish M. Mustard gas as a |
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injuries in military occupations, Aviat Space Environ Med, |
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cause of respiratory neoplasia in man, Lancet. 1968, 1: |
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2003; 74(9): 947-52. |
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1191. |
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C H A P T E R
50Trauma of Anterior Eye
Segment: An Update
Boris Malyugin(Russia)
Introduction
The division of the eye trauma to anterior and posterior is rather relative. Not infrequently anterior segment trauma is associated with the damage of the posterior eye structures including vitreous body, retina, choroid, sclera and optic nerve. More over traumatic influence leading to the anterior segment damage can compromise the eye but facial muscles, bones, brain, and other structures as well. That is why all traumatic cases require comprehensive examination of the eye and surrounding structures. In many cases of the eye injuries require urgent examination by physician and therapy.
Injuries of the Lids
INTRODUCTION
Lid injuries of various etiologies can be isolated or combined with traumatic changes of the eye and surrounding tissues. Lid lacerations are usually caused by bytes, or by sharp objects.
CLINICAL SIGNS AND SYMPTOMS
Direct blow to the eyelids cause blood infiltration of the lid tissues, echymosis, and may be associated with subconjunctival and orbital hemorrhages. In some cases, blood moves with the gravity from the lid to the check area.
In cases of laceration if it contains fat that means that the orbital septum has been perforated. The absence of the lid fold and blepharoptosis are the signs of the levator muscle damage.
Special attention should be pointed to the diagnosis of the orbital fractures. The latter is typically signaled by ecchymosis, lid swelling, proptosis, an in some cases ophthalmoplegia, subcutaneous emphysema from fracturing of the sinuses causing crepitation during palpation.
Orbital roof fractures can also be associated with liquior-rhinorrhea. Clinical suspicion of a blowout fracture is based on diagnosing one or more of the following symptoms: anesthesia of the nose and the skin of the lower lid, diplopia, pain at the upward gaze, displacement of the globe (downward or inward).
INVESTIGATIONS
As a first step the physician has to collect the history. Second step include the determining of the injury extent. Particular attention should be drawn to the underlying globe.
X-ray examination should be performed if the fracture of the orbit is suspected.
DIFFERENTIAL DIAGNOSIS
Lid hemorrhages usually does not have serious consequences but they can signal the injury of the orbital content which can be much more serious, for instance fracture of the roof of the orbit. Lid hematomas can also be associated with contusion injuries of the eye.
TREATMENT
Treatment is greatly depends of the extent of the injury. In cases of lid hemorrhage without damaging of the eye and other orbital structures optimal tactics will be to wait a period of time necessary for the for the spontaneous resorbtion of blood.
Bites (from humans or animals) should be cleared of the debris and irrigated with antiseptics and then allowed to heal with secondary tension. The use of prophylactic antibiotics is strongly recommended. In cases of animal bites (dogs, foxes, etc.) prophylaxis against rabies must be considered.
For lid lacerations primary repair with suturing should be performed. Careful reapproximation of all ruptured tissue planes and reconstruction of defects will ensure functional and cosmetic result.
312 |
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Clinical Diagnosis and Management of Ocular Trauma |
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Repair of the lid lacerations requires knowledge of |
INVESTIGATIONS |
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the anatomy. The lid is a triple-layered structure |
The examination can be performed with the penlight |
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composed of skin (anterior layer), orbicularis muscle |
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or under the slit lamp. Fluorescein drops or paper strips |
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(middle layer) and tarsus and palpebral conjunctiva |
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are very helpful in detecting the presence and extent |
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(posterior layer). All three layers of the lids should be |
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of epithelial defect. |
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closed separately. |
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During the |
lid reconstruction it |
is extremely |
DIFFERENTIAL DIAGNOSIS |
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important to save as much of the natural lid margin |
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A careful history must also be elucidated in order to |
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as possible. Special attention should be directed not |
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only to obtain the complete lid closure but also to repair |
find out the possibility of the presence of foreign bodies |
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the functional passage of tears with blinking into the |
and perforations. |
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lacrimal canaliculi and the lacrimal sac. In cases of |
In corneal epithelial defects differential diagnosis |
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damaged medial parts of the lids canaliculi should be |
should be performed with recurrent erosion due to the |
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carefully explored and reconstructed if necessary. |
damage of the epithelial basement membrane, herpes |
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If medial or lateral tarsal tendons were cut at the |
simplex keratitis, dry eyes, neurotrophic kertitis, atopic |
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time of trauma they should be identified and repaired. |
disease, ocular surface inflammation, damage to the |
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In the cases of conjunctival deficiency mucous |
limbal stem cells due to the chemical burns and limbal |
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membrane grafts taken from the contralateral eye or |
ischemia. |
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buccal cavity can be used with great success. |
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An orbital fracture in the absence of the physical |
TREATMENT |
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symptoms in many cases does not require operative |
Patients should be treated with antibiotics and |
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intervention. The most frequent indications for the |
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cycloplegics. A broad-spectrum antibiotic ointment |
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surgery are |
disabling dyplopia |
and severe |
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should be placed in the eye followed by placement |
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enophthalmos. Surgical intervention in orbital floor |
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of a semi-pressure patch on the eye. Use of ocular |
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fracture is not considered and emergency and usually |
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surface lubricants in small erosions may be enough to |
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delayed for 2 or more weeks. |
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improve patient comfort and support the healing |
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PROGNOSIS |
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process at the same time preventing infection. In eyes |
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with corneal abrasions corticosteroids are strictly |
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Lids tissue is a richly vascularized that is why it heals |
contraindicated. |
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rapidly. Primary repair of lid lacerations will produce |
In cases of foreign bodies located in the upper fornix |
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a very good cosmetic result. The latter depends on the |
the patient is seated and a drop of anesthetic is instilled. |
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extent and direction of the formed scar. On the other |
Then patient is asked to look down, the examiner |
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hand in delayer repair, presence of necrotic tissue and |
perform lid eversion and remove FB from the |
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after bites can delay healing and result in compromised |
conjunctival sac. |
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cosmetic appearance. Secondary reconstructive surgery |
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can be considered if this clinical situation arises. |
PROGNOSIS |
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In small corneal abrasions the prognosis is favorable. |
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Abrasions of the Globe |
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Epithelization is usually achieved in 24 to 48 hours. |
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INTRODUCTION |
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Blunt Injuries of the Globe |
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Corneal erosions are caused by eye scratching with |
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fingernails, hairbrushes, sand blowing in the air, |
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incorrect handling of the contact lenses, etc. The other |
INTRODUCTION |
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cause is the foreign body (FB) located under the upper |
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Blunt injuries of the globe can be caused by a variety |
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lid. |
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of objects that strikes the eye and disrupts its content. |
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CLINICAL SIGNS AND SYMPTOMS |
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Right after injury there is sudden onset of pain, lacrimation and blepharospasm. Eye motions as well as blinking can aggravate pain syndrome. Even at the absence of the FB, a foreign-body sensation is produced.
CLINICAL SIGNS AND SYMPTOMS
Conjunctival hemorrhage is the most common sign of ocular trauma (Fig. 50.1). By itself it has no consequences. In some cases severe bleeding can cause ballooning of the conjunctiva.
Trauma of Anterior Eye Segment: An Update |
313 |
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Fig. 50.1: Post-traumatic conjunctival hemorrhage |
Fig. 50.3: Traumatic iridodialysis secondary to blunt injury |
Fig. 50.2: Appearance of hyphema following blunt trauma |
Fig. 50.4: Traumatic cataract |
and iridodialysis |
|
secondary to blunt |
injury |
Hyphema is the other characteristic sign of the blunt eye trauma (Fig. 50.2). This term refers to blood retained in the anterior chamber. Some hyphemas are small and located in the inferiorly, while the others may fill the entire anterior chamber.
The extent of visual loss depends on the level of hyphema. In total hyphema when the entire anterior chamber is filled intraocular pressure is invariably elevated.
In the early post-traumatic period the aqueous humor contains cells and protein. Mild inflammation of uveal tissue may typically follow any trauma to the eye.
Hard blows of the eye typically produce iris sphincter rupture with traumatic mydriasis. The latter can be transitory or permanent. Traumatic iridodialysis of various extents may be one of the consequences of the blunt trauma (Fig. 50.3). Not infrequently iridodialysis is associated with traumatic cataract
(Fig. 50.4).
In blunt trauma pigment epithelium can be imprinted in the anterior surface of the lens forming a Vossius ring (Fig. 50.5). It is produced as the result
of forceful impact of the iris against the anterior surface of the lens. This sign is rather diagnostic and has no clinical significance and it is usually gradually resolves with time.
Blunt injury can cause acute or late cataract formation. Contusion cataract may form even in the absence of detectable damage of the capsule. Opacities usually localized in the anterior and/or posterior subcapsular region. Rosette-shaped cataract is often an early manifestation of lens contusion. It is located axially, involves posterior lens capsule, and can either improve spontaneously or progress to opacification of entire lens.
Blunt injury of the eye can also cause lens dislocation and subluxation (Fig. 50.6). The leading mechanism of this is the compression of the globe in axial direction with expansion in the equatorial plane leading to zonular rupture. The lens may be dislocated in the anterior chamber or in the vitreous cavity.
Location of the lens in the anterior chamber impedes the aqueous humor outflow and causes pupillary block glaucoma (Fig. 50.7). Iridodonesis is observed in cases of lens posterior dislocation when the patient moves the eye quickly.
314 |
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Clinical Diagnosis and Management of Ocular Trauma |
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INVESTIGATIONS |
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Medical history is a very important issue. Specific |
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ophthalmic tests include: refraction, visual acuity, |
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keratometry, biometry, B-scan ultrasonography, |
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gonioscopy. Slit-lamp microscopy is a major method |
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of eye examination. During examination pupil should |
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be maximally dilated. In all cases of blunt trauma |
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particular attention should be paid to fundus |
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examination. Physician has to evaluate not only affected |
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eye but also the fellow eye when possible. |
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DIFFERENTIAL DIAGNOSIS |
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Fig. 50.5: Vossius ring on the anterior capsule of the |
In blunt trauma scleral ruptures can be present without |
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eye with history of blunt trauma |
being visible to the examiner. Rupture is being suspected |
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when the eye is soft. |
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TREATMENT |
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A medication in conjunctival hemorrhage does not |
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speed up blood resorption. The latter usually occurs |
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within several days or weeks depending on the amount |
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of blood. In conjunctival ballooning it has to be kept |
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lubricated with ointment until the swelling diminishes. |
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In hyphemas medications inducing mydriasis and |
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cycloplegia are indicated together with sedation and |
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patching of the traumatized eye. In severe hyphemas |
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systemic aminocapronic acid in a dose of 50 mg/kg |
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can sharply decrease the incidence of rebleeding. In |
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Fig. 50.6: Dislocated cataractous lens following blunt trauma |
the hemorrhage does not resorb promptly, anterior |
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chamber lavage should be performed in order to |
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prevent blood staining of the cornea. |
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Careful monitoring of the intraocular pressure and |
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prompt treatment of ophthalmic hypertension are |
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mandatory. Beta-blockers, carbonic anhydrase |
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inhibitors and osmotic agents are widely used. |
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In cases of lens dislocation into the anterior chamber |
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leading to glaucoma emergency surgery is usually |
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indicated. Dislocation of the lens in the vitreous cavity |
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never requires emergency lens extraction. These |
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patients are managed surgically after inflammation |
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decrease. |
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The main treatment method of visually disabling |
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cataract is extraction. In general, traumatic cataracts |
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Fig. 50.7: Lens dislocated into anterior chamber |
can be safely removed with phacoemulsification |
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followed by posterior chamber intraocular lens |
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implantation. Indications for the surgical tactics in each |
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In blunt injuries even in cases when conjunctiva |
particular case vary extensively. |
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remains intact, rupture of sclera may occur. The most |
Risks of the modern small incision cataract surgery |
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common sites of the rupture are: limbal area, rectus |
are few if technically performed well. So the main source |
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muscle insertion and equator of the globe. |
of complications is the ocular comorbidity. Special |
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In patients with previous surgery (corneal trans- |
surgical techniques (vitrectomy, capsular tension rings, |
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plantation, radial keratotomy, cataract extraction) after |
pupil expansion devices) and alternative methods of |
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blunt trauma postoperative wound dehiscence can |
IOL fixation (i.e. scleral and iris fixation) should be |
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occur. |
considered since zonular dehiscence, loss of capsular |
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|
Trauma of Anterior Eye Segment: An Update |
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315 |
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integrity, small pupils and some other clinical findings |
segment are: conjunctival fornix of the upper or lower |
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|||||
and intraoperative events are not uncommon in |
lid, corneal epithelium and stroma, anterior chamber |
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traumatic cataract cases. |
and lens. |
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In corneal wound dehiscence, urgent surgery is |
Foreign body located on the corneal surface can |
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indicated. Suture placement can be combined with iris |
be single or multiple, clearly visible or detected only |
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|||||
reposition, cataract extraction, and hyphema washout |
with meticulous slit-lamp. Different biological or physical |
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if necessary. |
objects can be found (fragments of glass or metal, |
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fragments of insects, etc.). From the metal foreign bodies |
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PROGNOSIS |
rust, pieces of metal from grinding wheel, etc. are one |
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Hyphemas usually clear spontaneously. In some cases |
of the most often discovered. In metal objects a rust |
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ring can surround the foreign body. |
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of hyphemas rebleeding can occur. The highest |
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In perforating or penetrating injury aqueous humor |
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frequency of rebleeding is between 3 and 5 days after |
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enters the lens through the capsular defect. This results |
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initial trauma. In severe traumatic hyphemas glaucoma |
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in lens swelling, local opacification rapidly progressing |
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and corneal blood staining are the matters of concern. |
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to complete cataract formation (Fig. 50.8). If the |
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The latter can lead to persistent corneal opacity. |
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capsule defect |
is small |
it sometimes |
can heal |
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If total hyphema is the result of the secondary |
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spontaneously or can be blocked by the iris. In this |
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hemorrhage the prognosis is unfavorable. In cases when |
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cases localized lens opacity develops. |
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the lens is involved the prognosis of vision is reduced. |
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Perforating |
ocular |
injuries may |
lead to |
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In surgical reconstruction final visual acuity depends |
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endophthalmitis (Fig. 50.9). Characteristic clinical |
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on the retinal function. |
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signs of this condition are: lid edema, corneal haze, |
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Cataract removal usually leads to visual |
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aqueous inflammation, vitreous opacification, |
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rehabilitation. Nevertheless, ophthalmic co-morbidity |
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conjunctival hyperemia, edema and pain. |
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may prejudice good visual outcome. The final visual |
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acuity of patients with traumatic cataracts who undergo |
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surgery depends on a couple of factors including |
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amount of the initial eye damage, surgical trauma of |
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the ocular structures, and degree and duration of |
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postoperative inflammation. Proper medical |
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management of operated patients is essential for a |
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successful outcome of treatment. |
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Perforating Injuries of the Globe
Intraocular Foreign Bodies
INTRODUCTION
The physician must suspect the presence of the retained intraocular or intraorbital foreign body (FB) in all cases when periorbital or ocular tissues are lacerated.
CLINICAL SIGNS AND SYMPTOMS
Patients usually complain on the pain, photophobia, foreign body sensation, loss or decrease of vision. Lid swelling, tearing, eye redness, tissue defects at the wound entry site, corneal erosion, hyphema are the most common but not the only symptoms physician can observe. Local corneal defect and edema signals the site of perforation. Small sharp particles may pass through the cornea and sink inferiorly into the angle of the anterior chamber.
Clinical symptoms greatly depend on the localization of the FB. With the most common sites in the anterior
Fig. 50.8: An intralenticular metallic foreign body
Fig. 50.9: Bacterial endophthalmitis after ocular trauma
316 |
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|
Clinical Diagnosis and Management of Ocular Trauma |
|
|
INVESTIGATIONS |
|
all relevant factors. The risks of inflammation, toxic |
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|
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Patient’s history and detailed description of the injury |
chemical effects and fibrovascular proliferation should |
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be taken into consideration. |
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should be obtained. |
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These effects largely depend on the chemical nature |
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Single or double eversion of the lid is important |
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|
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of the FB. If the foreign body contains iron or |
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in the search and visualization of the FB located in the |
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|
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particularly copper treatment tactics should be |
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|
|
upper lid fornix. Direct visualization is very useful in |
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|
|
aggressive and early surgery is mandatory. The opposite |
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determining the presence and location of the foreign |
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|
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is true in small non-magnetic FB containing no or |
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body. It is sometimes very difficult to visualize small |
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|
|
minimal concentrations of aggressive substances. |
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|
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and transparent foreign bodies (for instance small |
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|
|
FB located in the anterior segment is not difficult |
||
|
|
particles of glass or plastic) even with the slit lamp. |
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|
|
to remove. In many cases anterior segment foreign |
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|
|
Iris defects due to perforation may be visible under |
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|
|
bodies can be removed through the wound of entry. |
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|
|
direct light or with transillumination. Examination of |
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|
|
If the object is small (2-3 mm in diameter) extraction |
||
|
|
the anterior chamber angle with the gonioscope can |
||
|
|
with magnet through the entry route may be considered. |
||
|
|
be useful in detecting small FB lying in the angle. |
||
|
|
Larger object can be removed utilizing the limbal |
||
|
|
Gonioscopy should be performed with caution not to |
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|
|
approach. |
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produce aqueous humor leak through the site of |
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|
|
Tears in the lens capsule of 2 mm in size can seal |
||
|
|
penetration. Ophthalmoscopy after maximal pupil |
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|
|
without causing cataractous changes. Thus small foreign |
||
|
|
dilation should be used in cases of suspected FB in |
||
|
|
bodies can be left in the lens. Bigger FB causing diffuse |
||
|
|
the vitreous or on the retina. |
||
|
|
cataracts should be managed during cataract extraction. |
||
|
|
In cases of opaque ocular media (extensive corneal |
||
|
|
edema, hyphema, cataract and vitreous hemorrhage) |
Intensive antibiotic treatment (topical, oral or IV) |
|
|
|
A- and B-scans, X-ray examination, computerized |
should be administered in all cases of intraocular FB. |
|
|
|
tomograms must be performed in suspected cases. |
With metal FB in the superficial corneal layers, after |
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|
|
Some of these examinations can also determine |
topical anesthesia is being applied, the patient is brought |
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|
|
whether or not the FB is magnetic. |
under slit lamp and the metal fragment is lifted with |
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|
|
the 25G needle on a syringe or a special instrument. |
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|
DIFFERENTIAL DIAGNOSIS |
Foreign body located in the deep corneal layers should |
|
|
|
be removed under the operating microscope. In cases |
||
|
|
Main differential diagnosis relates to the fact whether |
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|
|
of full thickness corneal penetrations suturing of the |
||
|
|
intraocular FB is present or not. Physician should keep |
||
|
|
wound should be done in order to achieve watertight |
||
|
|
in mind that multiple foreign bodies are not uncommon. |
||
|
|
seal. Postoperatively patients should be treated with |
||
|
|
The latter is characteristic to the explosions and blasting |
||
|
|
antibiotics and cycloplegics. |
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injuries (multiple intracorneal rocks), shotgun blasts and |
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the like. |
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PROGNOSIS |
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TREATMENT |
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Once the presence of the FB in the eye has been |
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established, the prognosis depends on the variety of |
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In cases of perforating |
ocular injuries prompt |
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factors. In the eye with the injury limited to the anterior |
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therapeutic intervention is justified. Local and systemic |
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eye segment prognosis is favorable in most cases and |
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wide spectrum antibiotics should be given. |
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depends of the effectiveness of the surgical repair and |
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Corticosteroids are administered in order to limit the |
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antibiotic treatment. In cases without good light |
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destructive effect of inflammation that accompanies |
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projection the prognosis is not infrequently poor. Foreign |
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infection. |
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bodies containing cooper or iron are particularly dange- |
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In most cases of globe lacerations urgent surgery |
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rous due to the chalcosis and siderosis development. |
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with the suturing of the wound site should be |
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Traumatic perforations of the cornea lead to scar |
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performed. |
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formation (Figs 50.10 and 50.11). |
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Clinical management in cases of FB largely depends |
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Consideration of the potential development of |
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of the judgment of the following factors: localization |
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sympathetic ophthalmia in perforating globe injury is |
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of the foreign body, its shape, size and composition, |
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extent of the trauma of surrounding tissues and the |
absolutely necessary. Sympathetic ophthalmia is more |
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decision of whether remove it or leave in place. |
likely in severe globe injury with excessive damage |
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The ophthalmologist must decide for or against |
of the uveal tissue leading to eye globe atrophy (Fig. |
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removal of the foreign body after careful judgment of |
50.12). |
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